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1.
J Cell Mol Med ; 28(13): e18508, 2024 Jul.
Article de Anglais | MEDLINE | ID: mdl-38953556

RÉSUMÉ

Both osteoporosis and tendinopathy are widely prevalent disorders, encountered in diverse medical contexts. Whilst each condition has distinct pathophysiological characteristics, they share several risk factors and underlying causes. Notably, oxidative stress emerges as a crucial intersecting factor, playing a pivotal role in the onset and progression of both diseases. This imbalance arises from a dysregulation in generating and neutralising reactive oxygen species (ROS), leading to an abnormal oxidative environment. Elevated levels of ROS can induce multiple cellular disruptions, such as cytotoxicity, apoptosis activation and reduced cell function, contributing to tissue deterioration and weakening the structural integrity of bones and tendons. Antioxidants are substances that can prevent or slow down the oxidation process, including Vitamin C, melatonin, resveratrol, anthocyanins and so on, demonstrating potential in treating these overlapping disorders. This comprehensive review aims to elucidate the complex role of oxidative stress within the interlinked pathways of these comorbid conditions. By integrating contemporary research and empirical findings, our objective is to outline new conceptual models and innovative treatment strategies for effectively managing these prevalent diseases. This review underscores the importance of further in-depth research to validate the efficacy of antioxidants and traditional Chinese medicine in treatment plans, as well as to explore targeted interventions focused on oxidative stress as promising areas for future medical advancements.


Sujet(s)
Antioxydants , Ostéoporose , Stress oxydatif , Espèces réactives de l'oxygène , Tendinopathie , Humains , Ostéoporose/métabolisme , Ostéoporose/thérapie , Ostéoporose/traitement médicamenteux , Antioxydants/usage thérapeutique , Tendinopathie/métabolisme , Tendinopathie/thérapie , Tendinopathie/anatomopathologie , Espèces réactives de l'oxygène/métabolisme , Animaux
2.
Front Endocrinol (Lausanne) ; 15: 1417007, 2024.
Article de Anglais | MEDLINE | ID: mdl-38952389

RÉSUMÉ

Ovarian aging is a complex process characterized by a decline in oocyte quantity and quality, directly impacting fertility and overall well-being. Recent researches have identified mitochondria as pivotal players in the aging of ovaries, influencing various hallmarks and pathways governing this intricate process. In this review, we discuss the multifaceted role of mitochondria in determining ovarian fate, and outline the pivotal mechanisms through which mitochondria contribute to ovarian aging. Specifically, we emphasize the potential of targeting mitochondrial dysfunction through innovative therapeutic approaches, including antioxidants, metabolic improvement, biogenesis promotion, mitophagy enhancement, mitochondrial transfer, and traditional Chinese medicine. These strategies hold promise as effective means to mitigate age-related fertility decline and preserve ovarian health. Drawing insights from advanced researches in the field, this review provides a deeper understanding of the intricate interplay between mitochondrial function and ovarian aging, offering valuable perspectives for the development of novel therapeutic interventions aimed at preserving fertility and enhancing overall reproductive health.


Sujet(s)
Vieillissement , Mitochondries , Ovaire , Humains , Femelle , Mitochondries/métabolisme , Vieillissement/physiologie , Vieillissement/métabolisme , Ovaire/métabolisme , Ovaire/physiologie , Animaux , Antioxydants/usage thérapeutique , Ovocytes/métabolisme , Ovocytes/physiologie , Mitophagie/physiologie
3.
Int J Nanomedicine ; 19: 6399-6425, 2024.
Article de Anglais | MEDLINE | ID: mdl-38952676

RÉSUMÉ

Myocardial infarction, usually caused by the rupture of atherosclerotic plaque, leads to irreversible ischemic cardiomyocyte death within hours followed by impaired cardiac performance or even heart failure. Current interventional reperfusion strategies for myocardial infarction still face high mortality with the development of heart failure. Nanomaterial-based therapy has made great progress in reducing infarct size and promoting cardiac repair after MI, although most studies are preclinical trials. This review focuses primarily on recent progress (2016-now) in the development of various nanomedicines in the treatment of myocardial infarction. We summarize these applications with the strategy of mechanism including anti-cardiomyocyte death strategy, activation of neovascularization, antioxidants strategy, immunomodulation, anti-cardiac remodeling, and cardiac repair.


Sujet(s)
Infarctus du myocarde , Nanomédecine , Infarctus du myocarde/thérapie , Humains , Animaux , Myocytes cardiaques/effets des médicaments et des substances chimiques , Antioxydants/usage thérapeutique , Nanostructures/usage thérapeutique , Nanostructures/composition chimique , Néovascularisation physiologique/effets des médicaments et des substances chimiques
4.
Chin J Dent Res ; 27(2): 169-174, 2024 Jun 28.
Article de Anglais | MEDLINE | ID: mdl-38953482

RÉSUMÉ

OBJECTIVE: To evaluate the effect of entrapment of curcumin within liposomal formulation and the sustained release attitude of the formulated liposomal gel on periodontal defects in diabetic patients in clinical and biochemical terms. METHODS: Thirty diabetic patients with periodontitis were randomly assigned to three equal groups and ten healthy participants were assigned as the control group. Group I was subjected to scaling and root planing (SRP) with application of sustained release liposomal curcumin gel. Group II was subjected to scaling and root planning with application of curcumin gel. Group III was subjected to scaling and root planning with application of placebo gel. Group IV (control group), no intervention was done. The following parameters were evaluated before treatment and after 6 and 12 weeks: plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment level (CAL), tumour necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1ß) and total antioxidant capacity (TAC). RESULTS: All study groups showed improvement in clinical and biochemical parameters that are statistically significant. Upon comparing the results of treatment modalities, the highest improvement was achieved in group I followed by group II then group III. CONCLUSION: Sustained release liposomal curcumin gel enhanced the antioxidant capacity, decreased the inflammatory mediators and showed more improvement in clinical outcome for treatment of periodontitis in diabetic patients.


Sujet(s)
Curcumine , Préparations à action retardée , Liposomes , Humains , Curcumine/usage thérapeutique , Curcumine/administration et posologie , Mâle , Femelle , Adulte d'âge moyen , Adulte , Détartrage dentaire , Parodontite/traitement médicamenteux , Surfaçage radiculaire , Résultat thérapeutique , Facteur de nécrose tumorale alpha , Antioxydants/usage thérapeutique , Antioxydants/administration et posologie , Indice parodontal
5.
BMC Nephrol ; 25(1): 226, 2024 Jul 15.
Article de Anglais | MEDLINE | ID: mdl-39009991

RÉSUMÉ

BACKGROUND: Contrast-induced acute kidney injury (CI-AKI) is an acute renal complication that occurs after intravascular contrast agent administration. Sodium selenite (SS) is an inorganic source of Se and has potent antioxidant properties. This study intends to examine its anti-inflammatory and antioxidant effects in CI-AKI. METHODS: A rat CI-AKI model was established with the pretreatment of SS (0.35 mg/kg). Hematoxylin-eosin staining was employed for histopathological analysis of rat kidney specimens. Biochemical analysis was conducted for renal function detection. Tissue levels of oxidative stress-related markers were estimated. Reverse transcription-quantitative polymerase chain reaction revealed the mRNA levels of proinflammatory cytokines. Western blotting showed the Nrf2 signaling-related protein expression in the rat kidney. RESULTS: SS administration alleviated the renal pathological changes and reduced the serum levels of serum creatinine, blood urea nitrogen, neutrophil gelatinase-associated lipocalin, cystatin C, and urinary level of kidney injury molecule-1 in CI-AKI rats. SS attenuated oxidative stress and inflammatory response in CI-AKI rat kidney tissues. SS activated the Nrf2 signaling transduction in the renal tissues of rats with CI-AKI. CONCLUSION: SS ameliorates CI-AKI in rats by reducing oxidative stress and inflammation via the Nrf2 signaling.


Sujet(s)
Atteinte rénale aigüe , Produits de contraste , Facteur-2 apparenté à NF-E2 , Stress oxydatif , Rat Sprague-Dawley , Transduction du signal , Sélénite de sodium , Animaux , Atteinte rénale aigüe/induit chimiquement , Atteinte rénale aigüe/métabolisme , Atteinte rénale aigüe/prévention et contrôle , Atteinte rénale aigüe/anatomopathologie , Stress oxydatif/effets des médicaments et des substances chimiques , Facteur-2 apparenté à NF-E2/métabolisme , Rats , Mâle , Produits de contraste/effets indésirables , Transduction du signal/effets des médicaments et des substances chimiques , Sélénite de sodium/pharmacologie , Sélénite de sodium/usage thérapeutique , Éléments de réponse aux anti-oxydants , Inflammation/métabolisme , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique , Créatinine/sang
6.
S D Med ; 77(2): 87-90, 2024 Feb.
Article de Anglais | MEDLINE | ID: mdl-38986163

RÉSUMÉ

Various medicinal agents aimed at improving Alzheimer disease (AD) include cholinesterase inhibitors, memantine, aducanumab, and antioxidants. These medications are typically prescribed once AD is diagnosed in the clinical setting in order to slow progression. Though initiating treatment after being diagnosed with AD is important, significance should be placed on recognizing known acquired risk factors in order to potentially decrease the likelihood of developing dementia and perhaps specifically AD. This article summarizes the acquired factors that influence risk for dementia.


Sujet(s)
Maladie d'Alzheimer , Démence , Humains , Maladie d'Alzheimer/traitement médicamenteux , Maladie d'Alzheimer/épidémiologie , Maladie d'Alzheimer/étiologie , Anticorps monoclonaux humanisés/usage thérapeutique , Antioxydants/usage thérapeutique , Anticholinestérasiques/usage thérapeutique , Démence/traitement médicamenteux , Démence/épidémiologie , Démence/étiologie , Mémantine/usage thérapeutique , Facteurs de risque
7.
Pharmacol Res Perspect ; 12(4): e1222, 2024 Aug.
Article de Anglais | MEDLINE | ID: mdl-38992963

RÉSUMÉ

Gentamicin is an aminoglycoside antibiotic with a rapid bactericidal effect on the treatment of many infections. However, its use at high concentrations for more than 7 days causes nephrotoxic side effects. This study investigated the potential of Resatorvid and alpha lipoic acid (ALA) in mitigating gentamicin-induced nephrotoxicity in rats, considering biochemical, histopathological, and molecular parameters. This study randomly distributed 34 Wistar albino rats into four groups: healthy control (n = 6), Gentamicin (80 mg/kg, n = 7), Gentamicin + Sham (%10 hydroalcoholic solution, n = 7), Gentamicin + Resatorvid (5 mg/kg, n = 7), and Gentamicin + ALA (100 mg/kg, n = 7). Resatorvid treatment led to a statistically significant decrease in urinary IL-18, KIM-1, and NGAL levels, whereas ALA treatment significantly reduced KIM-1 levels compared to the gentamicin-only group. Both Resatorvid and ALA showed partial reductions in urine creatinine levels. Moreover, treatments with Resatorvid and ALA resulted in statistically significant decreases in NRF-2, CAS-3, and NR4A2 expressions. However, only Resatorvid demonstrated a statistically significant decrease in NF-B expression. These findings highlight the potential of Resatorvid in ameliorating gentamicin-induced nephrotoxicity, thereby expanding the therapeutic utility of gentamicin and enhancing its efficacy against infections.


Sujet(s)
Antibactériens , Gentamicine , Rat Wistar , Acide lipoïque , Gentamicine/toxicité , Gentamicine/effets indésirables , Animaux , Acide lipoïque/pharmacologie , Acide lipoïque/usage thérapeutique , Rats , Antibactériens/effets indésirables , Antibactériens/pharmacologie , Mâle , Rein/effets des médicaments et des substances chimiques , Rein/anatomopathologie , Rein/métabolisme , Créatinine/sang , Créatinine/urine , Maladies du rein/induit chimiquement , Maladies du rein/traitement médicamenteux , Maladies du rein/anatomopathologie , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique , Molécules d'adhérence cellulaire
8.
Int J Mol Sci ; 25(13)2024 Jul 02.
Article de Anglais | MEDLINE | ID: mdl-39000393

RÉSUMÉ

Vitamin C is a water-soluble vitamin introduced through the diet with anti-inflammatory, immunoregulatory, and antioxidant activities. Today, this vitamin is integrated into the treatment of many inflammatory pathologies. However, there is increasing evidence of possible use in treating autoimmune and neoplastic diseases. We reviewed the literature to delve deeper into the rationale for using vitamin C in treating this type of pathology. There is much evidence in the literature regarding the beneficial effects of vitamin C supplementation for treating autoimmune diseases such as Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA) and neoplasms, particularly hematological neoplastic diseases. Vitamin C integration regulates the cytokines microenvironment, modulates immune response to autoantigens and cancer cells, and regulates oxidative stress. Moreover, integration therapy has an enhanced effect on chemotherapies, ionizing radiation, and target therapy used in treating hematological neoplasm. In the future, integrative therapy will have an increasingly important role in preventing pathologies and as an adjuvant to standard treatments.


Sujet(s)
Acide ascorbique , Maladies auto-immunes , Compléments alimentaires , Humains , Acide ascorbique/usage thérapeutique , Acide ascorbique/pharmacologie , Maladies auto-immunes/traitement médicamenteux , Maladies auto-immunes/immunologie , Animaux , Tumeurs hématologiques/thérapie , Tumeurs hématologiques/traitement médicamenteux , Tumeurs hématologiques/immunologie , Antioxydants/usage thérapeutique , Antioxydants/pharmacologie , Stress oxydatif/effets des médicaments et des substances chimiques
9.
J Pak Med Assoc ; 74(6): 1124-1129, 2024 Jun.
Article de Anglais | MEDLINE | ID: mdl-38948984

RÉSUMÉ

Objective: To compare the efficacy of tocotrienol and tocopherol in the management of patients with atherosclerotic cardiovascular diseases. METHODS: The systematic review was conducted in line with Preferred Reporting Items for Systematic Reviews and Meta- Analyses guidelines 2020, and comprised literature search from 2002 till January 5, 2023, on PubMed, Google Scholar, Cochrane Library, Google, Wiley-Inter Science Library, Medline, SpringerLink, Taylor and Francis databases. The search was conducted using key words, such as: "tocopherol", "tocotrienol", "vitamin E", "dyslipidaemia", "cardiovascular diseases" "cardioprotective", "hypercholesterolemia" and "atherosclerosis" along with Boolean operators. Human clinical studies regarding the use of tocotrienol or tocopherol or comparison of its efficacy in patients having atherosclerosis, dyslipidaemia leading to cardiovascular diseases, and studies including details of efficacy of any of the four alpha, beta, gamma, delta isomers of tocopherol or tocotrienol were included. Pertinent data from the eligible studies was retrieved and reviewed. RESULTS: Of the 516 articles identified, 26 (5%) articles met eligibility criteria. Of them 5(19%) were subjected to detailed analysis. Tocotrienol showed significant anti-oxidant efficacy at (250 mg/d) by decreasing cholesterol and serum inflammatory biomarkers i.e C-reactive protein (40%), malondialdehyde (34%), gamma-glutamyl transferase (22%) (p<0.001). Total anti-oxidant status (TAS) levels raised 22% (p<0.001) and Inflammatory cytokines i.e resistin, interleukin (IL)-1, IL-12, Interferon-gamma were decreased 15-17% (p<0.05-0.01) respectively by tocotrienol. Several microRNA (miRNA-133a, miRNA-223, miRNA-214, miRNA-155) were modulated by δ-tocotrienol. Whereas, tocopherol showed heterogeneity of results by either decreasing or increasing the risk of mortality in atherosclerotic cardiovascular diseases. Conclusion: Compared to tocopherol, tocotrienol was found to be safe and potential candidate for improving cardiovascular health in the management of atherosclerotic cardiovascular diseases.


Sujet(s)
Antioxydants , Athérosclérose , Tocophérols , Tocotriénols , Humains , Tocotriénols/usage thérapeutique , Tocotriénols/pharmacologie , Athérosclérose/traitement médicamenteux , Athérosclérose/prévention et contrôle , Tocophérols/usage thérapeutique , Antioxydants/usage thérapeutique , Maladies cardiovasculaires/prévention et contrôle , Dyslipidémies/traitement médicamenteux , Cholestérol/sang
10.
Molecules ; 29(13)2024 Jul 05.
Article de Anglais | MEDLINE | ID: mdl-38999158

RÉSUMÉ

Quercetin, a bioactive plant flavonoid, is an antioxidant, and as such it exhibits numerous beneficial properties including anti-inflammatory, antiallergic, antibacterial and antiviral activity. It occurs naturally in fruit and vegetables such as apples, blueberries, cranberries, lettuce, and is present in plant waste such as onion peel or grape pomace which constitute good sources of quercetin for technological or pharmaceutical purposes. The presented study focuses on the role of quercetin in prevention and treatment of dermatological diseases analyzing its effect at a molecular level, its signal transduction and metabolism. Presented aspects of quercetin potential for skin treatment include protection against aging and UV radiation, stimulation of wound healing, reduction in melanogenesis, and prevention of skin oxidation. The article discusses quercetin sources (plant waste products included), methods of its medical administration, and perspectives for its further use in dermatology and diet therapy.


Sujet(s)
Quercétine , Maladies de la peau , Quercétine/pharmacologie , Quercétine/usage thérapeutique , Quercétine/composition chimique , Humains , Maladies de la peau/traitement médicamenteux , Maladies de la peau/prévention et contrôle , Antioxydants/usage thérapeutique , Antioxydants/pharmacologie , Antioxydants/composition chimique , Extraits de plantes/composition chimique , Extraits de plantes/pharmacologie , Extraits de plantes/usage thérapeutique , Médecine préventive , Animaux , Composés phytochimiques/usage thérapeutique , Composés phytochimiques/composition chimique , Composés phytochimiques/pharmacologie , Cicatrisation de plaie/effets des médicaments et des substances chimiques
11.
Nutrients ; 16(13)2024 Jul 04.
Article de Anglais | MEDLINE | ID: mdl-38999888

RÉSUMÉ

Gastric cancer is an aggressive and multifactorial disease. Helicobacter pylori (H. pylori) is identified as a significant etiological factor in gastric cancer. Although only a fraction of patients infected with H. pylori progresses to gastric cancer, bacterial infection is critical in the pathology and development of this malignancy. The pathogenic mechanisms of this bacterium involve the disruption of the gastric epithelial barrier and the induction of chronic inflammation, oxidative stress, angiogenesis and metastasis. Adherence molecules, virulence (CagA and VacA) and colonization (urease) factors are important in its pathogenicity. On the other hand, resveratrol is a natural polyphenol with anti-inflammatory and antioxidant properties. Resveratrol also inhibits cancer cell proliferation and angiogenesis, suggesting a role as a potential therapeutic agent against cancer. This review explores resveratrol as an alternative cancer treatment, particularly against H. pylori-induced gastric cancer, due to its ability to mitigate the pathogenic effects induced by bacterial infection. Resveratrol has shown efficacy in reducing the proliferation of gastric cancer cells in vitro and in vivo. Moreover, the synergistic effects of resveratrol with chemotherapy and radiotherapy underline its therapeutic potential. However, further research is needed to fully describe its efficacy and safety in treating gastric cancer.


Sujet(s)
Infections à Helicobacter , Helicobacter pylori , Resvératrol , Tumeurs de l'estomac , Resvératrol/pharmacologie , Resvératrol/usage thérapeutique , Tumeurs de l'estomac/microbiologie , Tumeurs de l'estomac/traitement médicamenteux , Humains , Helicobacter pylori/effets des médicaments et des substances chimiques , Helicobacter pylori/pathogénicité , Infections à Helicobacter/traitement médicamenteux , Infections à Helicobacter/microbiologie , Prolifération cellulaire/effets des médicaments et des substances chimiques , Animaux , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique
12.
J Ovarian Res ; 17(1): 143, 2024 Jul 10.
Article de Anglais | MEDLINE | ID: mdl-38987824

RÉSUMÉ

BACKGROUND: This study was designed to examine the effect of resveratrol on mitochondrial biogenesis, oxidative stress (OS), and assisted reproductive technology (ART) outcomes in individuals with polycystic ovary syndrome (PCOS). METHODS: Fifty-six patients with PCOS were randomly assigned to receive 800 mg/day of resveratrol or placebo for 60 days. The primary outcome was OS in follicular fluid (FF). The secondary outcome involved assessing gene and protein expression related to mitochondrial biogenesis, mitochondrial DNA (mtDNA) copy number, and adenosine triphosphate (ATP) content in granulosa cells (GCs). ART outcomes were evaluated at the end of the trial. RESULTS: Resveratrol significantly reduced the total oxidant status (TOS) and oxidative stress index (OSI) in FF (P = 0.0142 and P = 0.0039, respectively) while increasing the total antioxidant capacity (TAC) (P < 0.0009). Resveratrol consumption also led to significant increases in the expression of critical genes involved in mitochondrial biogenesis, including peroxisome proliferator-activated receptor gamma coactivator (PGC-1α) and mitochondrial transcription factor A (TFAM) (P = 0.0032 and P = 0.0003, respectively). However, the effect on nuclear respiratory factor 1 (Nrf-1) expression was not statistically significant (P = 0.0611). Resveratrol significantly affected sirtuin1 (SIRT1) and PGC-1α protein levels (P < 0.0001 and P = 0.0036, respectively). Resveratrol treatment improved the mtDNA copy number (P < 0.0001) and ATP content in GCs (P = 0.0014). Clinically, the resveratrol group exhibited higher rates of oocyte maturity (P = 0.0012) and high-quality embryos (P = 0.0013) than did the placebo group. There were no significant differences between the groups in terms of chemical or clinical pregnancy rates (P > 0.05). CONCLUSIONS: These findings indicate that resveratrol may be a promising therapeutic agent for patients with PCOS undergoing assisted reproduction. TRIAL REGISTRATION NUMBER: http://www.irct.ir ; IRCT20221106056417N1; 2023 February 09.


Sujet(s)
Biogenèse des organelles , Syndrome des ovaires polykystiques , Techniques de reproduction assistée , Resvératrol , Humains , Femelle , Syndrome des ovaires polykystiques/traitement médicamenteux , Syndrome des ovaires polykystiques/métabolisme , Resvératrol/pharmacologie , Resvératrol/usage thérapeutique , Adulte , Stress oxydatif/effets des médicaments et des substances chimiques , Grossesse , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique , ADN mitochondrial/génétique , Mitochondries/effets des médicaments et des substances chimiques , Mitochondries/métabolisme , Cellules de la granulosa/effets des médicaments et des substances chimiques , Cellules de la granulosa/métabolisme
13.
J Ovarian Res ; 17(1): 138, 2024 Jul 04.
Article de Anglais | MEDLINE | ID: mdl-38965577

RÉSUMÉ

BACKGROUND: To investigate whether melatonin supplementation can enhance cardiometabolic risk factors, reduce oxidative stress, and improve hormonal and pregnancy-related factors in patients with PCOS. METHODS: We conducted a systematic search of PubMed/Medline, Scopus, and the Cochrane Library for articles published in English from inception to March 2023. We included randomized controlled trials (RCTs) on the use of melatonin for patients with polycystic ovary syndrome (PCOS). We performed a meta-analysis using a random-effects model and calculated the standardized mean differences (SMDs) and 95% confidence intervals (CIs). RESULTS: Six studies met the inclusion criteria. The result of meta-analysis indicated that melatonin intake significantly increase TAC levels (SMD: 0.87, 95% CI: 0.46, 1.28, I2 = 00.00%) and has no effect on FBS, insulin, HOMA-IR, TC, TG, HDL, LDL, MDA, hs-CRP, mFG, SHBG, total testosterone, and pregnancy rate in patients with PCOS compare to controls. The included trials did not report any adverse events. CONCLUSION: Melatonin is a potential antioxidant that may prevent damage from oxidative stress in patients with PCOS. However, the clear effect of melatonin supplementation on cardiometabolic risk factors, hormonal outcomes, and pregnancy-related outcomes needs to be evaluated further in large populations and long-term RCTs.


Sujet(s)
Facteurs de risque cardiométabolique , Compléments alimentaires , Mélatonine , Stress oxydatif , Syndrome des ovaires polykystiques , Essais contrôlés randomisés comme sujet , Humains , Mélatonine/pharmacologie , Mélatonine/usage thérapeutique , Syndrome des ovaires polykystiques/traitement médicamenteux , Syndrome des ovaires polykystiques/sang , Femelle , Stress oxydatif/effets des médicaments et des substances chimiques , Grossesse , Hormones/sang , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique , Antioxydants/administration et posologie
14.
An Acad Bras Cienc ; 96(3): e20230347, 2024.
Article de Anglais | MEDLINE | ID: mdl-39046019

RÉSUMÉ

Oxidative stress is involved in the pathogenesis of malaria, causing anemia, respiratory complications, and cerebral malaria. To mitigate oxidative stress, we investigated the effect of nutritional supplementation whit lycopene (LYC) on the evolution of parasitemia and survival rate in mice infected with Plasmodium berghei ANKA (Pb), comparing to the effects promoted by N-acetylcysteine (NAC). Therefore, 175 mice were randomly distributed into 4 groups; Sham: untreated and uninfected animals; Pb: animals infected with Pb; LYC+Pb: animals treated with LYC and infected with Pb; NAC+Pb: animals treated with NAC and infected with Pb. The animals were followed for 12 days after infection, and survival and parasitemia rates were evaluated. There was a 40.1% increase in parasitemia in the animals of the Pb group on the 12th day, and a survival rate of 45%. LYC supplementation slowed the development of parasitemia to 19% and promoted a significative increase in the survival rate of 80% on the 12th day after infection, compared to the Pb group, effects superior to those promoted by NAC, providing strong evidence of the beneficial effect of LYC on in vivo malaria and stressing the importance of antioxidant supplementation in the treatment of this disease.


Sujet(s)
Acétylcystéine , Antioxydants , Compléments alimentaires , Lycopène , Paludisme , Parasitémie , Plasmodium berghei , Animaux , Lycopène/usage thérapeutique , Lycopène/administration et posologie , Lycopène/pharmacologie , Parasitémie/traitement médicamenteux , Souris , Paludisme/traitement médicamenteux , Acétylcystéine/administration et posologie , Acétylcystéine/usage thérapeutique , Acétylcystéine/pharmacologie , Plasmodium berghei/effets des médicaments et des substances chimiques , Antioxydants/usage thérapeutique , Antioxydants/administration et posologie , Stress oxydatif/effets des médicaments et des substances chimiques , Caroténoïdes/usage thérapeutique , Caroténoïdes/administration et posologie , Mâle , Modèles animaux de maladie humaine , Répartition aléatoire
15.
Curr Drug Deliv ; 21(10): 1300-1319, 2024.
Article de Anglais | MEDLINE | ID: mdl-39034715

RÉSUMÉ

With the acceleration of people's pace of life, non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world, which greatly threatens people's health and safety. Therefore, there is still an urgent need for higher-quality research and treatment in this area. Nuclear factor Red-2-related factor 2 (Nrf2), as a key transcription factor in the regulation of oxidative stress, plays an important role in inducing the body's antioxidant response. Although there are no approved drugs targeting Nrf2 to treat NAFLD so far, it is still of great significance to target Nrf2 to alleviate NAFLD. In recent years, studies have reported that many natural products treat NAFLD by acting on Nrf2 or Nrf2 pathways. This article reviews the role of Nrf2 in the pathogenesis of NAFLD and summarizes the currently reported natural products targeting Nrf2 or Nrf2 pathway for the treatment of NAFLD, which provides new ideas for the development of new NAFLD-related drugs.


Sujet(s)
Produits biologiques , Facteur-2 apparenté à NF-E2 , Stéatose hépatique non alcoolique , Stéatose hépatique non alcoolique/traitement médicamenteux , Stéatose hépatique non alcoolique/métabolisme , Facteur-2 apparenté à NF-E2/métabolisme , Humains , Produits biologiques/pharmacologie , Produits biologiques/usage thérapeutique , Animaux , Stress oxydatif/effets des médicaments et des substances chimiques , Transduction du signal/effets des médicaments et des substances chimiques , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique
16.
Molecules ; 29(13)2024 Jun 28.
Article de Anglais | MEDLINE | ID: mdl-38999031

RÉSUMÉ

Tomatoes are well known for their impressive nutritional value among vegetables. However, the industrial processing of tomatoes generates a significant amount of waste. Specifically, 10% to 18% of the raw materials used in tomato processing become waste. This waste can seriously affect ecosystems, such as freshwater bodies, wetlands, rivers, and other natural environments, if not properly managed. Interestingly, tomato waste, specifically the skin, contains lycopene, a potent antioxidant and antimutagenic that offers a range of health benefits. This makes it a valuable ingredient in industries such as food and cosmetics. In addition, researchers are exploring the potential of lycopene in the treatment of various types of cancer. This systematic review, guided by the PRISMA 2020 methodology, examined studies exploring the possibility of tomato peel as a source of lycopene and carotenoids for cancer treatment. The findings suggest that tomato peel extracts exhibit promising anticancer properties, underscoring the need for further investigation of possible therapeutic applications. The compiled literature reveals significant potential for using tomato peel to create new cancer treatments, which could potentially revolutionize the field of oncology. This underscores the importance of continued research and exploration, emphasizing the urgency and importance of the scientific community's contribution to this promising area of study.


Sujet(s)
Lycopène , Tumeurs , Solanum lycopersicum , Solanum lycopersicum/composition chimique , Lycopène/composition chimique , Lycopène/pharmacologie , Humains , Tumeurs/traitement médicamenteux , Antioxydants/composition chimique , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique , Extraits de plantes/composition chimique , Extraits de plantes/pharmacologie , Extraits de plantes/usage thérapeutique , Caroténoïdes/usage thérapeutique , Caroténoïdes/composition chimique , Caroténoïdes/pharmacologie , Animaux
17.
Neuromolecular Med ; 26(1): 29, 2024 Jul 16.
Article de Anglais | MEDLINE | ID: mdl-39014255

RÉSUMÉ

Vascular dementia (VaD) is a cognitive disorder characterized by a decline in cognitive function resulting from cerebrovascular disease. The hippocampus is particularly susceptible to ischemic insults, leading to memory deficits in VaD. Astaxanthin (AST) has shown potential therapeutic effects in neurodegenerative diseases. However, the mechanisms underlying its protective effects in VaD and against hippocampal neuronal death remain unclear. In this study, We used the bilateral common carotid artery occlusion (BCCAO) method to establish a chronic cerebral hypoperfusion (CCH) rat model of VaD and administered a gastric infusion of AST at 25 mg/kg per day for 4 weeks to explore its therapeutic effects. Memory impairments were assessed using Y-maze and Morris water maze tests. We also performed biochemical analyses to evaluate levels of hippocampal neuronal death and apoptosis-related proteins, as well as the impact of astaxanthin on the PI3K/Akt/mTOR pathway and oxidative stress. Our results demonstrated that AST significantly rescued memory impairments in VaD rats. Furthermore, astaxanthin treatment protected against hippocampal neuronal death and attenuated apoptosis. We also observed that AST modulated the PI3K/Akt/mTOR pathway, suggesting its involvement in promoting neuronal survival and synaptic plasticity. Additionally, AST exhibited antioxidant properties, mitigating oxidative stress in the hippocampus. These findings provide valuable insights into the potential therapeutic effects of AST in VaD. By elucidating the mechanisms underlying the actions of AST, this study highlights the importance of protecting hippocampal neurons and suggests potential targets for intervention in VaD. There are still some unanswered questions include long-term effects and optimal dosage of the use in human. Further research is warranted to fully understand the therapeutic potential of AST and its application in the clinical treatment of VaD.


Sujet(s)
Apoptose , Démence vasculaire , Hippocampe , Troubles de la mémoire , Neurones , Neuroprotecteurs , Stress oxydatif , Rat Sprague-Dawley , Xanthophylles , Animaux , Xanthophylles/usage thérapeutique , Xanthophylles/pharmacologie , Hippocampe/effets des médicaments et des substances chimiques , Démence vasculaire/traitement médicamenteux , Rats , Mâle , Troubles de la mémoire/traitement médicamenteux , Troubles de la mémoire/étiologie , Stress oxydatif/effets des médicaments et des substances chimiques , Neurones/effets des médicaments et des substances chimiques , Apoptose/effets des médicaments et des substances chimiques , Neuroprotecteurs/usage thérapeutique , Neuroprotecteurs/pharmacologie , Protéines proto-oncogènes c-akt/métabolisme , Sérine-thréonine kinases TOR/métabolisme , Apprentissage du labyrinthe/effets des médicaments et des substances chimiques , Modèles animaux de maladie humaine , Transduction du signal/effets des médicaments et des substances chimiques , Phosphatidylinositol 3-kinases/métabolisme , Mort cellulaire/effets des médicaments et des substances chimiques , Antioxydants/usage thérapeutique , Antioxydants/pharmacologie , Test du labyrinthe aquatique de Morris/effets des médicaments et des substances chimiques
18.
Ageing Res Rev ; 99: 102416, 2024 Aug.
Article de Anglais | MEDLINE | ID: mdl-39002644

RÉSUMÉ

Alzheimer's disease (AD) is a fatal neurodegenerative disease in which senile plaques and neurofibrillary tangles are crucially involved in its physiological and pathophysiological processes. Growing animal and clinical studies have suggested that AD is also comorbid with some metabolic diseases, including type 2 diabetes mellitus (T2DM), and therefore, it is often considered brain diabetes. AD and T2DM share multiple molecular and biochemical mechanisms, including impaired insulin signaling, oxidative stress, gut microbiota dysbiosis, and mitochondrial dysfunction. In this review article, we mainly introduce oxidative stress and mitochondrial dysfunction and explain their role and the underlying molecular mechanism in T2DM and AD pathogenesis; then, according to the current literature, we comprehensively evaluate the possibility of regulating oxidative homeostasis and mitochondrial function as therapeutics against AD. Furthermore, considering dietary polyphenols' antioxidative and antidiabetic properties, the strategies for applying them as potential therapeutical interventions in patients with AD symptoms are assessed.


Sujet(s)
Maladie d'Alzheimer , Diabète de type 2 , Mitochondries , Stress oxydatif , Polyphénols , Transduction du signal , Maladie d'Alzheimer/métabolisme , Maladie d'Alzheimer/diétothérapie , Maladie d'Alzheimer/traitement médicamenteux , Diabète de type 2/métabolisme , Diabète de type 2/diétothérapie , Stress oxydatif/effets des médicaments et des substances chimiques , Humains , Polyphénols/pharmacologie , Polyphénols/usage thérapeutique , Transduction du signal/effets des médicaments et des substances chimiques , Transduction du signal/physiologie , Animaux , Mitochondries/métabolisme , Mitochondries/effets des médicaments et des substances chimiques , Phosphatidylinositol 3-kinases/métabolisme , Protéines proto-oncogènes c-akt/métabolisme , Antioxydants/usage thérapeutique
19.
Gynecol Endocrinol ; 40(1): 2381498, 2024 Dec.
Article de Anglais | MEDLINE | ID: mdl-39039898

RÉSUMÉ

N-acetylcysteine (NAC), a compound known for its cysteine and glutathione precursor properties, has been used in therapeutic applications for many years. Recently, there has been increasing interest in exploring the potential benefits of NAC in addressing polycystic ovary syndrome (PCOS). However, the exact mechanisms underlying NAC's therapeutic and clinical uses remain not fully understood. This review aims to specifically investigate how NAC offers protection against PCOS. This involved an extensive systematic review of the literature, and it made use of PubMed, Embase, and Web of Science databases. By analyzing key findings from over 100 research papers, the potential mechanisms through which NAC produces its effects were explored and summarized. Most studies suggest that NAC, whether used on its own or in combination with other medications, has the potential to counteract oxidative stress, utilize its anti-inflammatory and anti-apoptotic properties, and offer benefits in managing PCOS. Moreover, NAC might have the potential to influence specific signaling pathways in insulin target cells and ß cells. Diverse biological effects of NAC indicate its potential usefulness as a supplementary or therapeutic approach for managing PCOS. As a result, additional research is required to explore its potential in addressing PCOS.


Sujet(s)
Acétylcystéine , Antioxydants , Stress oxydatif , Syndrome des ovaires polykystiques , Syndrome des ovaires polykystiques/traitement médicamenteux , Syndrome des ovaires polykystiques/métabolisme , Acétylcystéine/usage thérapeutique , Acétylcystéine/pharmacologie , Humains , Femelle , Antioxydants/usage thérapeutique , Antioxydants/pharmacologie , Stress oxydatif/effets des médicaments et des substances chimiques
20.
Ren Fail ; 46(2): 2379008, 2024 Dec.
Article de Anglais | MEDLINE | ID: mdl-39034431

RÉSUMÉ

Despite efforts to find effective drugs for sepsis-associated acute kidney injury (SA-AKI), mortality rates in patients with SA-AKI have not decreased. Our study evaluated the protective effects of isoflavone osajin (OSJ) on SA-AKI in rats by targeting inflammation, oxidative stress, and apoptosis, which represent the cornerstones in the pathophysiological mechanism of SA-AKI. Polymicrobial sepsis was induced in rats via the cecal ligation and puncture (CLP) technique. Markers of oxidative stress were evaluated in kidney tissues using biochemical methods. The expression of interleukin-33 (IL-33), 8-hydroxydeoxyguanosine (8-OHdG), caspase-3, and kidney injury molecule-1 (KIM-1) was evaluated as indicators of inflammation, DNA damage, apoptosis, and SA-AKI respectively in the kidney tissues using immunohistochemical and immunofluorescent detection methods. The CLP technique significantly (p < 0.001) increased lipid peroxidation (LPO) levels and significantly (p < 0.001) decreased the activities of superoxide dismutase and catalase in kidney tissues. In the renal tissues, strong expression of IL-33, 8-OHdG, caspase-3, and KIM-1 was observed with severe degeneration and necrosis in the tubular epithelium and intense interstitial nephritis. In contrast, the administration of OSJ significantly (p < 0.001) reduced the level of LPO, markedly improved biomarkers of antioxidant status, decreased the levels of serum creatinine and urea, lowered the expression of IL-33, 8-OHdG, caspase-3, and KIM-1 and alleviated changes in renal histopathology. A promising binding score was found via a molecular docking investigation of the OSJ-binding mode with mouse IL-33 (PDB Code: 5VI4). Therefore, OSJ protects against SA-AKI by suppressing the IL-33/LPO/8-OHdG/caspase-3 pathway and improving the antioxidant system.


Sujet(s)
Atteinte rénale aigüe , Antioxydants , Apoptose , Rein , Simulation de docking moléculaire , Stress oxydatif , Sepsie , Animaux , Atteinte rénale aigüe/métabolisme , Atteinte rénale aigüe/étiologie , Atteinte rénale aigüe/traitement médicamenteux , Atteinte rénale aigüe/prévention et contrôle , Antioxydants/pharmacologie , Antioxydants/usage thérapeutique , Sepsie/complications , Sepsie/traitement médicamenteux , Rats , Stress oxydatif/effets des médicaments et des substances chimiques , Mâle , Apoptose/effets des médicaments et des substances chimiques , Rein/anatomopathologie , Anti-inflammatoires/pharmacologie , Anti-inflammatoires/usage thérapeutique , Isoflavones/pharmacologie , Isoflavones/usage thérapeutique , Modèles animaux de maladie humaine , Interleukine-33/métabolisme , Peroxydation lipidique/effets des médicaments et des substances chimiques , Caspase-3/métabolisme , Rat Sprague-Dawley , Molécules d'adhérence cellulaire
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