Fenpropathrin provoked kidney damage via controlling the NLRP3/Caspase-1/GSDMD-mediated pyroptosis: The palliative role of curcumin-loaded chitosan nanoparticles.

This study assessed the ability of formulated curcumin-loaded chitosan nanoparticles (CU-CS-NPs) to reduce the kidney damage resulting from fenpropathrin (FPN) in rats compared to curcumin (CU) in rats. Sixty male Sprague Dawley rats were separated into six groups and orally administered 1 mL/kg b.wt corn oil, 50 mg CU/kg b.wt, 50 mg CU-CS-NPs /kg b.wt., 15 mg FPN /kg b.wt, CU+ FPN or CU-CS-NPs + FPN for 60 days. Then, serum renal damage products were assessed. Total antioxidant capacity, reactive oxygen species, interleukin 1ß (IL-1ß), malondialdehyde, NF-κB P65, cleaved-Caspase-1, and Caspase-8 were estimated in kidney homogenates. The cleaved Caspase-3 and TNF-α immunoexpression and pyroptosis-related genes were determined in renal tissues. The results showed that CU-CS-NPS significantly repressed the FPN-induced increment in kidney damage products (urea, uric acid, and creatinine). Moreover, the FPN-associated hypo-proteinemia, renal oxidative stress and apoptotic reactions, and impaired renal histology were considerably repaired by CU and CU-CS-NPs. Additionally, compared to FPN-exposed rats, CU, and CU-CS-NPs-treated rats had considerably lower immunoexpression of cleaved Caspase-3 and TNF-α in renal tissue. The pyroptosis-related genes NLRP3, GSDMD, IL-18, Caspase-3, Caspase-1, IL-1ß, Caspase-8, TNF-α, and NF-κB dramatically upregulated by FPN exposure in the renal tissues. Yet, in CU and CU-CS-NPs-treated rats, the gene above expression deviations were corrected. Notably, CU-CS-NPs were superior to CU in preventing oxidative damage and inflammation and regulating pyroptosis in the renal tissues of the FPN-exposed group. The results of the present study conclusively showed the superior favorable effect of CU-CS-NPs in counteracting renal impairment linked to environmental pollutants.

Time-dependent expression of high-mobility group box-1 and toll-like receptors proteins as potential determinants of skin wound age in rats: Forensic implication.

The skin wound age determination in living subjects is an imperative task for forensic experts. In this study, we investigated the time-dependent expression of high-mobility group box-1 (HMGB1) and toll-like receptors 2 and 4 (TLR2 and 4) in rat skin wounds using real-time PCR and seek their forensic potentials during the skin wound repair process. In addition, the levels of serum pro-inflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6)), as well as nitric oxide (NO) production, were measured. The wound tissue and serum samples were collected after 30 min, 2 h, 6 h, 12 h, 1 day, 3 days, 5 days, and 7 days after incision. As a control (zero time), skin specimens and blood samples were collected without incision. The results reveal that the HMGB1, TLR2, and TLR4 expression levels were increased in a time-dependent manner until the first day where the peak level was achieved for the three tested genes compared with the zero time. On the 7th day, the statistical significance was lost for TLR2 and TLR4 but persisted for HMGB1. The serum TNF-α, IL6, and NO levels peaked within 30 min and 1st and 3rd day after injury, respectively. On the 7th day after incision, no significant differences exist in the TNF-α serum level compared to the control group, but the statistical significance persisted for IL6 and NO. It was apparent that the analyzed genes in the wound tissues showed higher R2 values rather than the serum biochemical indicators. Of note, a strong positive correlation was evident between the HMGB1 and that of TLR2 and TLR4 relative expression as well as IL-6 serum level. Conclusively, based on the observed changes in the analyzed markers in wound tissues and serum and R2 values obtained from mathematical models established to determine the wound age, the relative expression of HMGB1, TLR2, and TLR4 could be a reliable indicator for wound age determination in living subjects. Further investigation of these markers and mathematical models in human tissues is necessary.

The synbiotic mixture of Bacillus licheniformis and Saccharomyces cerevisiae extract aggravates dextran sulfate sodium induced colitis in rats.

BACKGROUND: Uncertain effects of probiotics and/or prebiotics have been reported in experimental and clinical colitis. This study aims to examine the effects of a synbiotic combination comprising Bacillus licheniformis DSM 17236 and Saccharomyces cerevisiae cell wall extract on dextran sulfate sodium (DSS)-induced colitis in Sprague Dawley rats. METHODS: Acute colitis was induced in rats by oral administration of DSS 3.5% for 7 days. Fifty rats were divided equally into five groups; one control group and the other groups were induced with colitis and treated with or without the tested synbiotic, mixed with diet, for 28 days and sulfasalazine (100 mg/kg) via intragastric tube once daily for 14 days. RESULTS: Symptomatically, the synbiotic administration raised the disease activity index (DAI) to comparable scores of the DSS group, specially from the 2nd to 7th days post DSS intoxication. It also induced a significant (p < 0.05) amplification of WBCs, myeloperoxidase (MPO), malondialdehyde (MDA), nuclear factor kappa B (NF-kB) expression and proinflammatory cytokines tumor necrosis factor alpha (TNFα), interferon gamma (INFγ), and interleukin-1 beta (IL-1ß) while depressed the antioxidant enzymes glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) when compared with the DSS and control groups. The DSS intoxicated and Synbiotic+DSS groups showed desquamations of the covering epithelium, noticeable diffuse leukocytic infiltrations, sever catarrhal enteritis, ischemic colitis with diffuse coagulative necrosis of the entire colonic mucosa. Contrarily, sulfasalazine proved to be effective in the reduction of the tested inflammatory markers and the pathological degenerative changes of the DSS ulcerative colitis. CONCLUSION: The examined synbiotic did not ameliorate but aggravated the DSS-induced colitis, so it should be subjected to intensive experimental and clinical testing before their use in animals and human.

Effect of hexavalent chromium exposure on the liver and kidney tissues related to the expression of CYP450 and GST genes of Oreochromis niloticus fish: Role of curcumin supplemented diet.

The present study evaluated the adverse effects of the hexavalent chromium (Cr (VI)) at sub-lethal concentrations and the ameliorative potential of curcumin (CUR) over a sub-chronic exposure period on Oreochromis niloticus. Fish were exposed to Cr (VI) (4.57 mg/L) and CUR (0.02% in diet or 200 mg/kg diet), individually or in combination for 60-days. The growth rate during the period of experiment, condition factor, body composition, hepatosomatic index (HSI), hematological parameters, oxidative stress, apoptotic and DNA damage, branchial, hepato- and nephrotoxicity were estimated in this study. Moreover, the changes in mRNA expression of Cytochromes (CYP450) and glutathione S-transferase (GST) in kidney and liver tissues were assessed by qRT-PCR. Additionally, the concentration of metallothionine in the liver, histological investigation, and lesion scoring to the branchial, hepatic, renal and gill tissues were applied. The results revealed that Cr (VI) exposure caused a significant decline in most hematological variables and growth rate with down-regulation of CYP450 and GST expression. Histologically, Cr (VI) induced diverse forms of cell injury, vascular, and inflammatory alterations with upregulation of caspase-3 and downregulation of Bcl2 expression in the examined tissues. Additionally, it elevated the levels of serum MDA and 8-hydroxy-2' -deoxyguanosine than control. CUR-supplementation resulted in a significant improvement in most indices, amelioration of histological alterations and up-regulation of CYP450 and GST expression. These results may conclude that dietary supplements with CUR could be useful for modulation of the growth with protective effects to the branchial, hepatic, and renal tissues in response to Cr (VI) exposure, thereby presenting a promising feed additive for Nile tilapia in aquaculture.

Food Yellow4 reprotoxicity in relation to localization of DMC1 and apoptosis in rat testes: Roles of royal jelly and cod liver oil.

Food Yellow 4 (FY4) is a lemon-yellow-colored synthetic organic azo dye, which is used widely for imparting pleasant and attractive appearance to foods and cosmetics. The present study aimed at evaluating the possible mechanism underlying the FY4-induced reprotoxicity in rats, and the potential supportive role of royal jelly (RJ) or cod liver oil (CLO), which is a natural remedy with several pharmacological benefits, against induced toxicity. Forty-eight male rats were divided into different groups-the control group, the CLO group (0.4 mL/kg), the RJ group (300 mg/kg), the FY4 group (500 mg/kg b.w.), and the co-treated groups (FY4 + CLO or FY4 + RJ). Semen analysis, serum hormones, and enzyme activities were estimated. Immunohistochemical staining was performed using anti-PCNA, anti-Sox 9, anti-STRA8, anti-DMC1, and anti-ssDNA antibody. The FY4 group exhibited a significant decrease in sperm concentration and motility percentage (%) and a substantial reduction in the TES and LH levels. Testicular LDH, ACP, and SDH were observed to be inhibited. Furthermore, co-localization of DMC1 and ssDNA, which reflected apoptotic induction in the leptotene and zygotene spermatocytes, respectively, was observed to have markedly elevated in the FY4 treated rats, with fewer PCNA-positive and SOX9-positive cells and higher ssDNA-positive cells in the seminiferous epithelium in comparison to the control groups. Interestingly, co-treatment with CLO or RJ exhibited healthy sperms and restored their features, activated the enzyme production, and raised the levels of sexual hormones. In addition, both RJ and CLO restored the features of the testicular tissue as observed under a light microscope, and limited the apoptosis as observed through antibody staining. Collectively, the results of the present study revealed that the co-administration of RJ or CLO with FY4 improved the biochemical, hormonal, and structural aspects of the testicular tissue in rats. Therefore, CLO and RJ may be considered promising agents that would be able to improve the testicular structure and function in the FY4-exposed individuals.

Fenpropathrin induces testicular damage, apoptosis, and genomic DNA damage in adult rats: Protective role of camel milk.

Fenpropathrin (FNP) is a member of the synthetic pyrethroids. Herein, the present study was conducted to investigate, for the first time, the potentially harmful effects of FNP on the reproductive system of male rats. In addition, the prophylactic or concurrent influence of camel milk (CM) was assessed. Adult male rats were divided into five groups; control, vehicle control (oil), CM (2ml/rat/day), FNP (15mg/kg bwt/60 days), CM/FNP (prophylaxis) and FNP /CM (co-treated) groups. Sperm morphology, count, serum testosterone (TES), luteinizing hormone (LH) and follicle-stimulating hormone (FSH), thiobarbituric acid reactive substances (TBARS), total antioxidant capacity (TAC), superoxide dismutase (SOD), testicular enzymes, and comet assay analysis were estimated. In addition, histopathology, the ultrastructure of testicular tissue and apoptosis were evaluated. Reduced body weight and gonadosomatic index were observed in the FNP exposed group. TES, LH, FSH were markedly declined following FNP treatment. SOD and TAC concentrations were reduced while PC and TBARS were significantly elevated in FNP group indicating oxidative stress. Furthermore, FNP induced DNA damage and apoptosis in the testis which was evidenced histopathologically and by electron microscope examination. CM significantly counteracted FNP reprotoxic effects, particularly at the prophylactic routine (CM/FNP) than the co-exposure (FNP/CM) one. Conclusively, these findings verified that CM could be a potential candidate therapy against FNP reprotoxic impacts.

Understanding fenpropathrin-induced pulmonary toxicity: What apoptosis, inflammation, and pyreptosis reveal analyzing cross-links at the molecular, immunohistochemical, and immunofluorescent levels.

Fenpropathrin (FN), a pyrethroid has been linked to potential pulmonary toxic effects to humans via incident direct or indirect ingestion. Thus, we aimed to the investigate the underlying mechanisms of lung toxicity upon exposure to FN in the rat model, besides studying whether curcumin (CCM) and curcumin-loaded chitosan nanoformulation (CCM-Chs) can mitigate FN-induced lung damage. Six distinct groups, namely, control, CCM, CCM-Chs, FN, and CCM + FN, CCM-Chs + FN were assigned separately. The inflammatory, apoptotic, and oxidative stress states, histological, immunohistochemical, and immunofluorescence examination of different markers within the pulmonary tissue were applied. The results revealed that the FN-induced tissue damage might be caused by the oxidative stress induction and depressed antioxidant glutathione system in the lungs of rats. Furthermore, FN upregulated the expression of genes related to inflammation, and pyroptosis, and elevated the immunoreactivity of Caspase-3, tumor necrosis factor-α, vimentin, and 4-Hydroxynonenal in pulmonary tissues of FN-exposed rats compared to the control. CCM and CCM-Chs mitigated the FN-induced disturbances, while remarkably, CCM-Chs showed better potency than CCM in mitigating the FN-induced toxicity. In conclusion, this study shows the prominent preventive ability of CCM-Chs more than CCM in combatting the pulmonary toxicity induced by FN. This may be beneficial in developing therapeutic and preventive strategies against FN-induced pulmonary toxicity.

Pulmonary damage induction upon Acrylic amide exposure via activating miRNA-223-3p and miRNA-325-3p inflammasome/pyroptosis and fibrosis signaling pathway: New mechanistic approaches of A green-synthesized extract.

Exposure to acrylic amide (AD) has garnered worldwide attention due to its potential adverse health effects, prompting calls from the World Health Organization for intensified research into associated risks. Despite this, the relationship between oral acrylic amide (acrylamide) (AD) exposure and pulmonary dysfunction remains poorly understood. Our study aimed to investigate the correlation between internal oral exposure to AD and the decline in lung function, while exploring potential mediating factors such as tissue inflammation, oxidative stress, pyroptosis, and apoptosis. Additionally, we aimed to evaluate the potential protective effect of zinc oxide nanoparticles green-synthesized moringa extract (ZNO-MONPs) (10mg/kg b.wt) against ACR toxicity and conducted comprehensive miRNA expression profiling to uncover novel targets and mechanisms of AD toxicity (miRNA 223-3P and miRNA 325-3P). Furthermore, we employed computational techniques to predict the interactions between acrylic amide and/or MO-extract components and tissue proteins. Using a rat model, we exposed animals to oral acrylamide (20mg/kg b.wt for 2 months). Our findings revealed that AD significantly downregulated the expression of miRNA 223-3P and miRNA 325-3P, targeting NLRP-3 & GSDMD, respectively, indicating the induction of pyroptosis in pulmonary tissue via an inflammasome activating pathway. Moreover, AD exposure resulted in lipid peroxidative damage and reduced levels of GPX, CAT, GSH, and GSSG. Notably, AD exposure upregulated apoptotic, pyroptotic, and inflammatory genes, accompanied by histopathological damage in lung tissue. Immunohistochemical and immunofluorescence techniques detected elevated levels of indicative harmful proteins including vimentin and 4HNE. Conversely, concurrent administration of ZNO-MONPs with AD significantly elevated the expression of miRNA 223-3P and miRNA 325-3P, protecting against oxidative stress, apoptosis, pyroptosis, inflammation, and fibrosis in rat lungs. In conclusion, our study highlights the efficacy of ZNO-MONPs NPs in protecting pulmonary tissue against the detrimental impacts of foodborne toxin AD.

Green Synthesized Zinc Oxide Nanoparticles Using Moringa olifera Ethanolic Extract Lessens Acrylamide-Induced Testicular Damage, Apoptosis, and Steroidogenesis-Related Gene Dysregulation in Adult Rats.

This study assessed the possible protective role of green synthesized zinc oxide nanoparticles using Moringa olifera leaf extract (MO-ZNPs) in acrylamide (ACR)-induced reproductive dysfunctions in male rats. ACR (20 mg/kg b.wt/day) and/or MO-ZNPs (10 mg/kg b.wt/day) were given orally by gastric gavage for 60 days. Then, sperm parameters; testicular enzymes; oxidative stress markers; reproductive hormones including testosterone, luteinizing hormone (LH)-estradiol, and follicle-stimulating hormone (FSH) concentration; testis histology; steroidogenesis-related gene expression; and apoptotic markers were examined. The findings revealed that MO-ZNPs significantly ameliorated the ACR-induced decline in the gonadosomatic index and altered the pituitary-gonadal axis, reflected by decreased serum testosterone and FSH with increased estradiol and LH, and sperm analysis disruption. Furthermore, a notable restoration of the tissue content of antioxidants (catalase and reduced glutathione) but depletion of malondialdehyde was evident in MO-ZNPs+ACR-treated rats compared to ACR-exposed ones. In addition, MO-ZNPs oral dosing markedly rescued the histopathological changes and apoptotic caspase-3 reactions in the testis resulting from ACR exposure. Furthermore, in MO-ZNPs+ACR-treated rats, ACR-induced downregulation of testicular steroidogenesis genes and proliferating cell nuclear antigen (PCNA) immune-expression were reversed. Conclusively, MO-ZNPs protected male rats from ACR-induced reproductive toxicity by suppressing oxidative injury and apoptosis while boosting steroidogenesis and sex hormones.

Exploring cardiac impact of oral nicotine exposure in a transplantable Neoplasm Mice Model: Insights from biochemical analysis, morphometry, and molecular docking: Chlorella vulgaris green algae support.

Nicotine-induced cardiac tissue damage is a concern for cancer patients, but the exact pathogenesis from nicotine oral exposure is unclear. This study was designed to investigate the impact of nicotine and Chlorella vulgaris (Ch. V) on cardiac glutathione homeostasis, inflammatory response, cardiac damage markers, apoptotic proteins and histopathological findings in an experimentally transplantable neoplasm mouse model (Ehrlich ascites carcinoma; EAC). In the in-vivo experiment, the female Swiss mice were divided into four groups: control, Ch.V (100 mg/kg), Nicotine (100 µg/ml/kg), and a combination group ( Nocotine+ Ch.V) for 40 days. Furthermore, in this study,the effects of C. vulgaris components on caspase-3, TNF-α, and IL-1ß activity were explored using Molecular Operating Environment (MOE) docking software to ensure its ability to counteract the toxic effects of nicotine. The results indicated that nicotine has induced significant (P < 0.001) cardiopathic alterations in EAC-bearing mice with changes in cardiac tissue enzymes. C. Vulgaris attenuated the nicotine-induced cardiac glutathione inhibition, suppressed the inflammatory response, exerted antiapoptotic effects, mitigated myocardial injury biomarkers, and repaired cellular and tissue damage. Moreover, the molecular docking results revealed the ability of C. vulgaris to bind with interleukin-1 receptor type 1 (IL1R1) and tumor necrosis factor receptor superfamily member 1 A (TNFRSF1A) in the mice tissues, ameliorating apoptosis and inflammatory processes associated with nicotine-induced cardiotoxicity. This study provides a model for understanding nicotine-induced myocardial injury during experimentally transplantable neoplasm. It highlights C. vulgaris as a beneficial food supplement for cancer patients exposed to nicotine orally.

Curcumin-loaded chitosan nanoparticles alleviate fenpropathrin-induced hepatotoxicity by regulating lipogenesis and pyroptosis in rats.

In this study, the probable alleviative role of curcumin (CMN) (50 mg/kg b.wt) or curcumin-loaded chitosan nanoparticle (CLC-NP) (50 mg/kg b.wt) was assessed against the hepatotoxic effect of a widely used pyrethroid insecticide, fenpropathrin (FEN) (15 mg/kg b.wt) in rats in a 60-day experiment. The results revealed that CMN and CLC-NP significantly suppressed the FEN-induced increment in serum hepatic enzyme activities (ALT, AST, and ALP) and hyperbilirubinemia. Moreover, FEN-associated dyslipidemia, hepatic oxidative stress, and altered hepatic histology were significantly rescued by CMN and CLC-NP. Furthermore, the increased TNF-α and Caspase-3 immunoexpression in hepatic tissues of FEN-exposed rats was significantly reduced in CMN and CLC-NP-treated ones. FEN exposure significantly upregulated the pyroptosis-related genes, including GSDMD, Casp-1, Casp-3, Casp-8, IL-18, TNF-α, IL-1ß, and NF-κB and altered the expression of lipogenesis-related genes including SREBP-1c, PPAR-α, MCP1, and FAS in the hepatic tissues. Nevertheless, the earlier disturbances in gene expression were corrected in CMN and CLC-NP-treated groups. Of note, compared to CMN, CLC-NP was more effective at inhibiting oxidative damage and controlling lipogenesis and pyroptosis in the hepatic tissues of FEN-exposed rats. Conclusively, the current study findings proved the superior and useful role of CLC-NP in combating pollutants associated with hepatic dysfunction.

Comparative Assessment of Three Medicinal Plants against Diabetes and Oxidative Stress Using Experimental and Computational Approaches.

The hilly and rural areas' people of Bangladesh have a great history of putting into use numerous traditional medicinal plants to cure diseases. Therefore, with ethanol extract of Molineria capitulata (EEMC), methanol extract of Trichosanthes tricuspidata (METT), and methanol extract of Amorphophallus campanulatus (MEAC), we mandate evaluation of in vitro α-amylase inhibition, antioxidants, and molecular docking, and ADMET/T analysis. According to iodine starch methods, α-amylase inhibition was performed, and quantitative total phenolic and flavonoid content was determined by established methods, whereas DPPH free radical scavenging and reducing power assays were performed in previously established protocols, respectively. A comparative study among three plants (EEMC, METT, and MEAC) possessed a significant (p < 0.01) effect but EEMC showed the highest impact on enzyme inhibition. Plants in the measuring phenolic content METT and flavonoid measurement MEAC displayed most potent in the same way in the DPPH test was METT, and in reducing power capability MEAC has showed the highest effect between three extracts. Docking's study also reveals the compounds of METT (Cyclotricuspidoside A and Cyclotricuspidoside C) exhibit the superior score among all the compounds. This finding indicates that EEMC, METT, and MEAC substantially impact α-amylase inhibition along with antioxidants. In silico study also reveals the potency of these plants, but further in-depth, precise molecular studies are needed.

Evaluation of Antidiabetic Activity of Oxadiazole Derivative in Rats.

The oxadiazole ring has long been used for the treatment of several diseases. This study aimed to analyze the antihyperglycemic and antioxidant roles of the 1,3,4-oxadiazole derivative with its toxicity. Diabetes was induced through intraperitoneal administration of alloxan monohydrate at 150 mg/kg in rats. Glimepiride and acarbose were used as standards. Rats were divided into groups of normal control, disease control, standard, and diabetic rats (treated with 5, 10, and 15 mg/kg of 1,3,4-oxadiazole derivative). After 14 days of oral administration of 1,3,4-oxadiazole derivatives (5, 10, and 15 mg/kg) to the diabetic group, the blood glucose level, body weight, glycated hemoglobin (HbA1c), insulin level, antioxidant effect, and histopathology of the pancreas were performed. The toxicity was measured by estimating liver enzyme, renal function, lipid profile, antioxidative effect, and liver and kidney histopathological study. The blood glucose and body weight were measured before and after treatment. Alloxan significantly increased blood glucose levels, HbA1c, alanine transaminase, aspartate aminotransferase, urea, cholesterol, triglycerides, and creatinine. In contrast, body weight, insulin level, and antioxidant factors were reduced compared to the normal control group. Treatment with oxadiazole derivatives showed a significant reduction in blood glucose levels, HbA1c, alanine transaminase, aspartate aminotransferase, urea, cholesterol, triglycerides, and creatinine as compared to the disease control group. The 1,3,4-oxadiazole derivative significantly improved body weight, insulin level, and antioxidant factors compared to the disease control group. In conclusion, the oxadiazole derivative showed potential antidiabetic activity and indicated its potential as a therapeutic.

Comparable bio-evaluation of curcumin and chitosan-encapsulated curcumin nanoparticles against the reprotoxic potential of fenpropathrin pyrethroid in rats: Genomic and morphometric prospectives.

This study delves into the intricate exploration of potential toxic effects resulting from subchronic exposure to fenpropathrin (FNP) on the reproductive system of male SD rats. Adding to the novelty, our study undertakes a pioneering comparison of the effects of curcumin (CUR) and curcumin-encapsulated chitosan nanoparticles (CS.CUR.NPs) on these toxic effects. The study involved a cohort of sixty male SD rats (six groups): vehicle control, CUR, Cs.CUR.NPs, FNP, and two combination groups (FNP with CUR or Cs.CUR.NPs). The synthesized Cs.CUR.NPs nanoparticles underwent meticulous characterization using Fourier Infrared spectroscopy (FT-IR) and transmission electron microscopy (TEM). The findings revealed that FNP caused oxidative stress, sperm abnormalities, reduced motility and sperm count FNP decreased serum LH, FSH, 17-ß estradiol, and testosterone levels. FNP downregulated the mRNA expression of the spermatogenesis and steroidogenesis-related genes, While, downregulated hypothalamic KISS-1 and KISS-1r expression. Histopathological alterations were assessed and scored. Surprisingly, the treatment with CUR and Cs.CUR.NPs exhibited remarkable restorative effects on semen quality, sex hormone levels, antioxidant capacity, and mRNA expression of the targeted genes. Notably, Cs.CUR.NPs displayed superior properties when compared to CUR. Nevertheless, further research is imperative to evaluate their efficacy across various bodily tissues.

Enhancement of biochemical and genomic pathways through lycopene-loaded nano-liposomes: Alleviating insulin resistance, hepatic steatosis, and autophagy in obese rats with non-alcoholic fatty liver disease: Involvement of SMO, GLI-1, and PTCH-1 genes.

Non-alcoholic fatty liver (NAFL) is a prevalent hepatic disorder of global significance that can give rise to severe complications. This research endeavor delves into the potential of nano-liposomal formulated Lycopene (Lip-Lyco) in averting the development of obesity and insulin resistance, both of which are major underlying factors contributing to NAFL. The investigation further scrutinizes the impact of Lip-Lyco on intricate cellular pathways within the liver tissue of rats induced with NAFL, specifically focusing on the progression of steatosis and fibrosis. To establish an obesity-NAFL model, twenty rats were subjected to a high-fat diet (HFD) for a duration of twelve weeks, after which they received an oral treatment of Lip-Lyco (10mg/kg) for an additional eight weeks. Another group of sixteen non-obese rats were subjected to treatment with or without Lip-Lyco, serving as a control for comparison. Results: The rats on a hypercaloric diet had high body mass index (BMI) and insulin resistance, reflected in disturbed serum adipokines and lipid profiles. Oxidative stress, inflammation, and apoptosis were evident in hepatic tissue, and the autophagic process in hepatocytes was inhibited. Additionally, the hedgehog pathway was activated in the liver tissue of NAFL group. Lip-Lyco was found to counteract all these aspects of NAFL pathogenesis. Lip-Lyco exhibited antioxidant, anti-inflammatory, hypoglycemic, antiapoptotic, autophagy-inducing, and Hedgehog signaling inhibitory effects. This study concludes that Lip-Lyco, a natural compound, has promising therapeutic potential in combating NAFLdisease. However, more experimental and clinical studies are required to confirm the effectiveness of lycopene in treating NAFLdisease.

Palliative effect of Moringa olifera-mediated zinc oxide nanoparticles against acrylamide-induced neurotoxicity in rats.

Repeated acrylamide (ACR) exposure in experimental animals and humans causes variable degrees of neuronal damage. Because of its unique features, several green synthesized nanomaterials are explored for neuromodulatory activity. Hence, this study investigated the effect of green synthesized zinc oxide nanoparticles using Moriga olifera leaves extract (MO-ZnONP) against acrylamide (ACR)-induced neurobehavioral and neurotoxic impacts in rat. Forty male Sprague Dawley rats were distributed into four groups orally given distilled water, MO-ZnONP (10 mg/kg b.wt), ACR (20 mg/kg b.wt), or MO-ZnONP + ACR for 60 days. Gait quality and muscular, motor, and sensory function were assessed. Acetylcholinesterase (AChE), dopamine, catalase, malondialdehyde (MDA), and Zn brain contents were determined. Brain histopathology and immunohistochemical localization of the amyloid-ß protein and abnormal Tau were performed. The results revealed that MO-ZnONP significantly reduced ACR-induced sensory dysfunctions, hind limb abnormality, and motor deficits. Additionally, the ACR-induced increase in dopamine and AChE were significantly supressed by MO-ZnONP. Besides, MO-ZnONP significantly restored catalase and Zn content but reduced increased MDA brain content resulting from ACR. Furthermore, the ACR-induced neurodegenerative changes and increased amyloid-ß and phosphorylated Tau immunoexpression was significantly abolished by MO-ZnONP. Conclusively, MO-ZnONP could be used as a biologically effective compound for mitigating ACR's neurotoxic and neurobehavioral effects.

Liposome-Encapsulated Berberine Alleviates Liver Injury in Type 2 Diabetes via Promoting AMPK/mTOR-Mediated Autophagy and Reducing ER Stress: Morphometric and Immunohistochemical Scoring.

In the advanced stages of type 2 diabetes mellitus (T2DM), diabetic liver damage is a common complication that can devastate a patient's quality of life. The present study investigated the ability of liposomal berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM) and the possible pathways by which it does so. Liver tissue microarchitectures and immunohistochemical staining were applied during the study. The rats were divided into a control non-diabetic group and four diabetic groups, which are the T2DM, T2DM-Lip-BBR (10 mg/kg b.wt), T2DM-Vildagliptin (Vild) (10 mg/kg b.wt), and T2DM-BBR-Vild (10 mg/kg b.wt + Vild (5 mg/kg b.wt) groups. The findings demonstrated that Lip-BBR treatment could restore liver tissue microarchitectures, reduce steatosis and liver function, and regulate lipid metabolism. Moreover, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats. Lip-BBR also activated the GLP-1 expression, which stimulated insulin biosynthesis. It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation. Collectively, Lip-BBR ameliorated diabetic liver injury in a T2DM rat model with its promotion activity of AMPK/mTOR-mediated autophagy and limiting ER stress.

Green Synthesized Zinc Oxide Nanoparticles Attenuate Acrylamide-Induced Cardiac Injury via Controlling Endoplasmic Reticulum Stress-Associated Apoptosis Through ATF3/CHOP/BCL2 Signaling in Rats.

Due to their distinctive properties, several eco-friendly metal oxide nanoparticles were assessed for their possible cardioprotective properties. Acrylamide (ACD), a pervasive chemical in food and the environment, has been linked to cardiac toxicity. Therefore, this study examined the probable protective effect of green synthesized zinc oxide nanoparticles (GS-ZNPs) against ACD-oral exposure-induced cardiac damage in rats. For 60 days, 40 male Sprague-Dawley rats were separated into four sets that orally administered distilled water, 10-mg GS-ZNP/kg b.w., 20-mg ACD/kg b.w., or GS-ZNP + ACD. Then, cardiac damage indicators comprising CPK, CK-MB, cTn, and LDH were assessed. Besides, cardiac tissues' architecture, oxidative stress indicators, and Zn content were evaluated. The mRNA expression of the ERS-related genes, including ATF3, ATF4, ATF6, XBP-1, CHOP, JNKs, and BiP, were determined. Moreover, ERS-dependent anti-apoptotic (BCL-2) and apoptotic (Caspase-3 and BAX) genes mRNA expression were analyzed. The results showed that GS-ZNP significantly alleviated the increased ACD-induced serum cardiac damage indicators, MDA tissue content, and histopathological changes. Furthermore, the ACD-induced reduction of antioxidants and Zn heart contents were significantly reestablished by GS-ZNP. Furthermore, the ACD-induced upregulation of the ERS-encoding genes and apoptotic genes was reversed by GS-ZNP. Besides, the ACD-induced BCL-2 downregulation was counteracted by GS-ZNP. Overall, GS-ZNP could be a biologically potent compound to alleviate ACD's cardiotoxic effects, possibly by controlling the ERS and apoptosis-related genes and antioxidant activity.

Concerns with Male Infertility Induced by Exposure to Titanium Nanoparticles and the Supporting Impact of Pelargonium graveolens Essential Oil: Morphometric Records in Male-Wistar Rats.

Background: Due to the increased use of titanium dioxide nanoparticles (TiO2 NPs), the risks of their reprotoxic effect arise. This study anticipated examining the potential protective effects of GEO (geranium essential oil) components screened via GC/MS analysis against the reprotoxic impacts of TiO2 NPs on male rats. Methods: Thirty-two adult male rats were randomly assigned to four groups: control, GEO (75 mg/kg bwt/orally/day/60 days), TiO2 NPs (100 ppm/rat/IP/day/60 days), and TiO2 NPs + GEO. After 60 days, hormonal assay, semen appraisal, lipid peroxidation, antioxidant enzymes, testis and prostate morphometry, and the steroidogenesis-related genes' mRNA expressions were assessed. Results: The TEM and DLS results demonstrated that synthesized TiO2 NPs are spherical with minimal aggregations polydispersed and varying in size from 50 to 100 nm. TiO2 NPs IP injection-induced sperm abnormalities decreased the percent of motile sperms in the sperm count, reduced sex hormone levels, altered the testicular oxidant/antioxidant status and mRNA expression of steroid-related genes, and induced architectural alterations in testicular, epididymal, and prostate gland tissues. GEO significantly rescued the TiO2 NPs-altered spermiogram, sex hormones, and antioxidant capacity, restored the tissue architectures, and enhanced steroidogenesis-related gene mRNA expression. Conclusions: These findings may significantly contribute to developing combinatorial treatments for infertility associated with various environmental and industrial xenobiotic exposures.

Sustained Functioning Impairments and Oxidative Stress with Neurobehavioral Dysfunction Associated with Oral Nicotine Exposure in the Brain of a Murine Model of Ehrlich Ascites Carcinoma: Modifying the Antioxidant Role of Chlorella vulgaris.

Background: This study provides a model for studying the mechanism(s) responsible for the nervous tissue damage and misfunctioning that occurred due to oral nicotine exposure, considered a stress factor, during the presence of Ehrlich ascites carcinoma bearing in the mouse model (EAC). The mitigating role of Chlorella vulgaris (CV) against nicotine-induced brain damage was evaluated. Methods: Eighty Swiss female mice were classified into four groups, these were the control, the CV group, the nicotine group(100 µg/kg), and the combination group. Oxidant/antioxidant status, proinflammatory cytokines levels, DNA damage, quantitative microscopical lesions, and Caspase 3, Bcl-2 proteins were assessed in the current study. Levels of dopamine (DA) and gamma-aminobutyric acid (GABA) were also evaluated. Results: Nicotine was found to cause pronounced neurobehavioral alterations, increase the mortalities oxidative stress DNA damage, and augment the inflammatory response in brain tissue alongside the microstructural alteration. The administration of CV with nicotine in EAC-bearing mice rescued the detrimental effects of nicotine. Conclusions: CV aids in reducing the harmful effects of nicotine and returns the conditions caused by nicotine to near-control levels. Thus, we are in favor of giving it to cancer patients who are taking daily dosages of nicotine even by smoking cigarettes or being exposed to second-hand smoke.