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The advanced non-small cell lung cancer (NSCLC) that harbors epidermal growth factor receptor (EGFR) mutations has put a selective pressure on the discovery and development of newer EGFR inhibitors. Therefore, the present study intends to explore the pharmacological effect of Araguspongine C (Aragus-C) as anticancer agent against lung cancer. The effect of Aragus-C was evaluated on the viability of the A549 and H1975 cells. Further biochemical assays were performed to elaborate the effect of Aragus-C, on the apoptosis, cell-cycle analysis, and mitochondrial membrane potential in A549 cells. Western blot analysis was also conducted to determine the expression of EGFR in A549 cells. Tumor xenograft mice model from A549 cells was established to further elaborate the pharmacological activity of Aragus-C. Results suggest that Aragus C showed significant inhibitory activity against A549 cells as compared to H1975 cells. It has been found that Aragus-C causes the induction of apoptosis and promotes cell-cycle arrest at the G2/M phase of A549 cells. It also showed a reduction in the overexpression of EGFR in A549 cells. In tumor xenograft mice model, it showed a significant reduction of tumor volume in a dose-dependent manner, with maximum inhibitory activity was reported by the 8 mg/kg treated group. It also showed significant anti-inflammatory and antioxidant activity by reducing the level of TNF-α, IL-1ß, IL-6, and MDA, with a simultaneous increase of superoxide dismutase and glutathione peroxidase. We have demonstrated the potent anti-lung cancer activity of Aragus-C, and it may be considered as a potential therapeutic choice for NSCLC treatment.
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Apoptosis , Receptores ErbB , Neoplasias Pulmonares , Estrés Oxidativo , Ensayos Antitumor por Modelo de Xenoinjerto , Humanos , Receptores ErbB/metabolismo , Receptores ErbB/genética , Receptores ErbB/antagonistas & inhibidores , Animales , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/patología , Neoplasias Pulmonares/metabolismo , Apoptosis/efectos de los fármacos , Células A549 , Estrés Oxidativo/efectos de los fármacos , Ratones , Ratones Desnudos , Inflamación/tratamiento farmacológico , Inflamación/metabolismo , Inflamación/patología , Ratones Endogámicos BALB C , Antineoplásicos/farmacología , Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Carcinoma de Pulmón de Células no Pequeñas/patología , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Línea Celular TumoralRESUMEN
Ischemia-reperfusion (IR) injury remains a pivotal contributor to myocardial damage following acute coronary events and revascularization procedures. Phosphoinositide 3-kinase (PI3K), a key mediator of cell survival signaling, plays a central role in regulating inflammatory responses and cell death mechanisms. Trans-chalcone (Tch), a natural compound known for its anti-inflammatory activities, has shown promise in various disease models. The aim of the current study was to investigate the potential protective effects of Tch against myocardial injury induced by ischemia and reperfusion challenges by targeting the PI3K-inflammasome interaction. Experimental models utilizing male rats subjected to an in vivo model of IR injury and myocardial infarction were employed. Administration of Tch (100 µg/kg, intraperitoneally) significantly reduced myocardial injury, as indicated by limited infarct size and decreased levels of the myocardial enzyme troponin. Mechanistically, Tch upregulated PI3K expression, thereby inhibiting the activity of the NOD-like receptor protein 3 inflammasome followed by the activation of pro-inflammatory cytokines interleukin-1ß (IL-1ß) and IL-18. Moreover, it mitigated oxidative stress and suppressed vascular-intercellular adhesion molecules, contributing to its cardioprotective effects. The PI3K/Akt pathway inhibitor LY294002 considerably attenuated the beneficial effects of Tch. These findings highlight the therapeutic potential of Tch in ameliorating myocardial injury associated with IR insults through its modulation of the PI3K/Akt-inflammasome axis. The multifaceted mechanisms underlying its protective effects signify Tch as a promising candidate for further exploration in developing targeted therapies aimed at mitigating ischemic heart injury and improving clinical outcomes in cardiovascular diseases characterized by IR injury.
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Daño por Reperfusión Miocárdica , Fosfatidilinositol 3-Quinasas , Proteínas Proto-Oncogénicas c-akt , Ratas Sprague-Dawley , Animales , Masculino , Daño por Reperfusión Miocárdica/tratamiento farmacológico , Daño por Reperfusión Miocárdica/metabolismo , Daño por Reperfusión Miocárdica/prevención & control , Daño por Reperfusión Miocárdica/patología , Proteínas Proto-Oncogénicas c-akt/metabolismo , Ratas , Fosfatidilinositol 3-Quinasas/metabolismo , Inflamasomas/metabolismo , Inflamasomas/efectos de los fármacos , Chalcona/farmacología , Chalcona/análogos & derivados , Chalcona/uso terapéutico , Transducción de Señal/efectos de los fármacos , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismoRESUMEN
TNF-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily that is capable of apoptosis induction selectively in tumor cells. Although TRAIL has been harnessed in numerous clinical trials, resistance to TRAIL-induced apoptosis is a major challenge ahead of this therapy in various cancer models as well as in leukemia. Since histone deacetylases (HDACs) are known to affect drug resistance in malignant cells, the present study aimed to evaluate the potential of fisetin for sensitization of MOLT-4 and K-562 leukemic cells to TRAIL-induced apoptosis. The MOLT-4 and K-562 cells were treated with increasing concentrations of fisetin and its impact on the growth inhibition and apoptosis induction of TRAIL were evaluated by MTT and Annexin V/7-AAD assays. The impact of fisetin on the mRNA and protein expression levels of apoptosis regulatory genes such as BIRC2/c-IAP1, CFLAR/cFLIP, CASP3, CASP7, CASPP9, TNFRSF10A/DR4, TNFRSF10B/DR5, and BID were examined by PCR array, qRT-PCR, and flow cytometry. Pre-treatment of MOLT-4 and K-562 cells with fisetin reduced the IC50 of TRAIL in growth inhibition along with an improvement in apoptosis induction by TRAIL. The expression of the BIRC2 gene encoding antiapoptotic protein c-IAP1 downregulated in the fisetin-treated cells while the expressions of TNFRSF10A and TNFRSF10B encoding TRAIL death receptors increased. Fisetin demonstrated a potential for alleviating the TRAIL resistance by modulating the apoptosis regulatory factors and improving the expressions of TRAIL receptors that could facilitate the application of TRAIL in cancer therapies.
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PURPOSE: Reflux esophagitis is a condition characterized by inflammation and irritation of the esophagus, resulting from the backflow of stomach acid and other gastric contents into the esophagus. Columbianadin is a coumarin derivative that exhibits anti-inflammatory and antioxidant effects. In this study, we tried to scrutinize the protective effect of Columbianadin against acute reflux esophagitis in rats. METHODS: RAW 264.7 cells were utilized to assess cell viability and measure the production of inflammatory parameters. The rats received anesthesia, and reflux esophagitis was induced via ligation of pylorus and fore stomach and corpus junction. Rats received the oral administration of Columbianadin (25, 50 and 100 mg/kg) and omeprazole (20 mg/kg). The gastric secretion volume, acidity, and pH were measured. Additionally, the levels of oxidative stress parameters, cytokines, and inflammatory markers were determined. At the end of the study, mRNA expression was assessed. RESULTS: Columbianadin remarkably suppressed the cell viability and production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and prostaglandin (PGE2). Columbianadin treatment remarkably suppressed the secretion of gastric volume, total acidity and enhanced the pH level in the stomach. Columbianadin remarkably altered the level of hydrogen peroxidase, free iron, calcium, and plasma scavenging activity, sulfhydryl group; oxidative stress parameters like malonaldehyde, glutathione, superoxide dismutase, catalase, glutathione peroxidase; inflammatory cytokines viz., TNF-α, IL-6, IL-1ß, IL-10, IL-17, and monocyte chemoattractant protein-1; inflammatory parameters including PGE2, iNOS, COX-2, and nuclear kappa B factor (NF-κB). Columbianadin remarkably (P < 0.001) suppressed the mRNA expression TNF-α, IL-6, IL-1ß and plasminogen activator inhibitor-1. CONCLUSIONS: Columbianadin demonstrated a protective effect against acute reflux esophagitis via NF-κB pathway.
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Esofagitis Péptica , FN-kappa B , Estrés Oxidativo , Animales , Esofagitis Péptica/tratamiento farmacológico , FN-kappa B/metabolismo , FN-kappa B/efectos de los fármacos , Masculino , Ratas , Estrés Oxidativo/efectos de los fármacos , Citocinas/metabolismo , Modelos Animales de Enfermedad , Supervivencia Celular/efectos de los fármacos , Enfermedad Aguda , Células RAW 264.7 , Ratones , Ratas Wistar , Transducción de Señal/efectos de los fármacos , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Antiinflamatorios/farmacología , Antiinflamatorios/uso terapéuticoRESUMEN
Ischemic stroke is a leading cause of human mortality. Cerebral ischemia-reperfusion injury (CI/RI) is a primary cause of stroke. Ischemia-reperfusion (I/R) resulting in oxidative stress and inflammatory events may lead to severe neuronal impairments. Thus, anti-oxidative and anti-inflammatory mediators that can alleviate post-I/R neuronal injuries are required for the treatment of CI/RI. An alkaloid, voacangine (VCG) is a recognized antioxidant, anti-inflammatory, and anticancer agent. Hence, the current study intended to explore the neuroprotective potential and the principal mechanisms of VCG in CI/RI. The experimental rats were divided into four sets: control, I/R-induced, I/R + VCG (2.5 mg/kg), I/R + VCG (5 mg/kg). CI/RI was induced by implanting a thread into the middle cerebral artery occlusion (MCAO) model. Brain damages were assessed on the basis of brain edema, brain infarct volume, neurological deficit score, histopathology, oxidative stress, and neuroinflammation. Results revealed that VCG inhibited the triggering of NLRP3 inflammasome, pro-inflammatory cytokines, lipid peroxidation, but enhanced the antioxidant status in MCAO rats. Furthermore, VCG treatment averted brain damage by I/R, neuroinflammation, and oxidative stress by suppressing NF-κBp65/MAPK pathways. The results of the study provide pertinent insights pertaining to the role of VCG as a potential neuroprotective agent against ischemic stroke.
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Infarto de la Arteria Cerebral Media , Fármacos Neuroprotectores , Estrés Oxidativo , Daño por Reperfusión , Animales , Estrés Oxidativo/efectos de los fármacos , Daño por Reperfusión/tratamiento farmacológico , Masculino , Infarto de la Arteria Cerebral Media/tratamiento farmacológico , Ratas , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/uso terapéutico , Ratas Sprague-Dawley , Enfermedades Neuroinflamatorias/tratamiento farmacológico , Isquemia Encefálica/tratamiento farmacológico , Factor de Transcripción ReIA/metabolismo , Transducción de Señal/efectos de los fármacos , Sistema de Señalización de MAP Quinasas/efectos de los fármacosRESUMEN
The purpose of this research was to investigate whether or not avicularin (AVL) possesses any anticancer properties when tested against lung cancer. In the beginning, the effect that it had on the cellular viability of A549 cells was investigated, and it was discovered that AVL has a considerable negative impact on cellular viability. Following that, an investigation using flow cytometry was carried out to investigate its function in the process of apoptosis and the cell cycle of A549 cells. It has been discovered that AVL significantly promotes apoptosis and stops the cell cycle at the G2/M phase. The colony-forming capacity of A549 cells was observed to be greatly suppressed as the AVL concentration increased compared to the group that received no treatment. In addition to this, the benzo(a)pyrene in vivo model was established in order to investigate the pharmacological value of AVL. The findings revealed that AVL greatly prevented the formation of pro-inflammatory cytokines, in addition to the reduction in oxidative stress, which was evidenced by a reduction in the concentration of TNF-α, IL-1ß, IL-6, and MDA with an improvement in the concentration of SOD and GPx, respectively. Our results successfully demonstrated the pharmacological benefit of avicularin against lung cancer, and it has been suggested that it showed a multifactorial effect.
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Apoptosis , Inflamación , Neoplasias Pulmonares , Estrés Oxidativo , Estrés Oxidativo/efectos de los fármacos , Humanos , Apoptosis/efectos de los fármacos , Neoplasias Pulmonares/patología , Neoplasias Pulmonares/tratamiento farmacológico , Células A549 , Animales , Inflamación/patología , Inflamación/tratamiento farmacológico , Supervivencia Celular/efectos de los fármacos , Citocinas/metabolismo , RatonesRESUMEN
Straw mulching incorporation has a wide range of environmental benefits that make it an effective practice for sustainable agro-ecosystem in the semi-arid regions. There is an urgent need to improve the 13C-photosynthates distribution, water use efficiency (WUE) and maize canopy characteristics under the diverse tillage practices with straw mulched management strategies for sustainable intensification of maize production. The field study consists of three diverse tillage systems (RT: rotary tillage; CT, conventional tillage; MT, minimum tillage) with three straws mulching (NS: no straw mulch; SS: straw mulch on the soil surface; SI: straw incorporated into the soil) were assessed under the ridge-furrow rainfall harvesting system. Our results showed that the rotary tillage with straw incorporated into the soil significantly reduces the ET rate (11 %), and leaf rolling index; as a result considerably improves LAI, LEI, 13C-photosynthates distribution, N accumulation, and above ground biomass under various growth stages. The RTSI treatment significantly improved soil water storage, soil organic carbon (52 %, SOC), soil C storage (39 %, SCS), and NPK nutrients uptake (70 %, 62 %, and 69 %) of maize than observed for the rest of all other treatments, respectively. The RTSI treatment improves soil water balance, grain yield (53 %), biomass yield (37 %), WUEg (51 %), WUEb (35 %), nutrients uptake, and mitigating soil water depletion than the MTNS treatment. Although RTSS can achieve optimal soil water storage in the short term, RTSI has a great potential in improving soil carbon stability, canopy characteristics, soil water storage, and WUE, contributing to sustainable and intensive corn production in agricultural ecosystems in semi-arid regions.
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PURPOSE: To determine the effect of gallic acid or its combination with glibenclamide on some biochemical markers and histology of the cornea of streptozotocin (STZ) induced diabetic rats. METHODS: Following induction of diabetes, 24 male albino rats were divided into four groups of six rats each. Groups 1 and 2 (control and diabetic) received rat pellets and distilled water; group 3 (gallic acid) received rat pellets and gallic acid (10 mg/kg, orally) dissolved in the distilled water; and group 4 (gallic acid + glibenclamide) received rat pellets, gallic acid (10 mg/kg, orally), and glibenclamide (5 mg/kg, orally) dissolved in the distilled water. The treatments were administered for three months after which the rats were sacrificed after an overnight fast. Blood and sera were collected for the determination of biochemical parameters, while their eyes were excised for histology. RESULTS: STZ administration to the rats induced insulin resistance, hyperglycemia, microprotenuria, loss of weight, oxidative stress, inflammation, and alteration of their cornea histology, which was abolished following supplementation with gallic acid or its combination with glibenclamide. CONCLUSIONS: The study showed the potentials of gallic acid and glibenclamide in mitigating systemic complication and histological changes in the cornea of diabetic rats induced with STZ.
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Diabetes Mellitus Experimental , Gliburida , Ratas , Masculino , Animales , Gliburida/efectos adversos , Hipoglucemiantes/efectos adversos , Ácido Gálico/efectos adversos , Estreptozocina/efectos adversos , Diabetes Mellitus Experimental/complicaciones , Diabetes Mellitus Experimental/tratamiento farmacológico , Córnea/patología , Agua/efectos adversos , GlucemiaRESUMEN
Osteoarthritis (OA) is characterized by the gradual deterioration and worsening of the knee joint, leading to both pain and deformity. The current research exhibited the anti-osteoarthritis effect of lusianthridin against monosodium iodoacetate (MIA) induced OA in rats. RAW cells were used for the cell viability. The inflammatory cytokines and mediators were estimated in the cell lines after the lipopolysaccharide (LPS) treatment. For the in vivo study, the rats were received the intraperitoneal administration of MIA (3 mg/kg) for the induction of OA. The rats were received the oral administration of lusianthridin (5, 10 and 20 mg/kg) and the body and organ weight estimated. Antioxidant, cytokines, inflammatory and matrix metalloproteinases (MMP) level were also estimated. The mRNA expression of MMP were also estimated. The lusianthridin treatment remarkably suppressed the cell viability. LPS induced RAW cell suppressed the level of nitrate, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), prostaglandin (PGE2), MMP-2 and MMP-9 level. Lusianthridin remarkably altered the level of body weight and organ weight (liver, spleen, renal and heart weight). lusianthridin suppressed the oxidative stress via altered the level of antioxidant parameters. Lusianthridin significantly (p < 0.001) decreased the level of cartilage oligometrix matrix protein (COMP) and c-reactive protein (CRP); cytokines such as TNF-α, IL-1ß, IL-6, IL-10; inflammatory parameters include 5- Lipoxygenase (5-LOX), COX-2, leukotriene B4 (LTB4), PGE2; transforming growth factor beta (TGF-ß); MMP level like MMP-1, 3, 9, 13, respectively. Lusianthridin significantly suppressed the mRNA expression of MMP. Collectively, the result of the study showed that antiosteoarthritis effect of lusianthridin via suppression of inflammatory parameters.
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Osteoartritis , Factor de Necrosis Tumoral alfa , Ratas , Animales , Ácido Yodoacético/toxicidad , Antioxidantes/farmacología , Interleucina-6 , Dinoprostona , Ciclooxigenasa 2/genética , Ciclooxigenasa 2/metabolismo , Lipopolisacáridos , Osteoartritis/inducido químicamente , Osteoartritis/tratamiento farmacológico , Osteoartritis/metabolismo , Citocinas/metabolismo , Interleucina-1beta/genética , ARN MensajeroRESUMEN
Purpose: To determine the effect of gallic acid or its combination with glibenclamide on some biochemical markers and histology of the cornea of streptozotocin (STZ) induced diabetic rats. Methods: Following induction of diabetes, 24 male albino rats were divided into four groups of six rats each. Groups 1 and 2 (control and diabetic) received rat pellets and distilled water; group 3 (gallic acid) received rat pellets and gallic acid (10 mg/kg, orally) dissolved in the distilled water; and group 4 (gallic acid + glibenclamide) received rat pellets, gallic acid (10 mg/kg, orally), and glibenclamide (5 mg/kg, orally) dissolved in the distilled water. The treatments were administered for three months after which the rats were sacrificed after an overnight fast. Blood and sera were collected for the determination of biochemical parameters, while their eyes were excised for histology. Results: STZ administration to the rats induced insulin resistance, hyperglycemia, microprotenuria, loss of weight, oxidative stress, inflammation, and alteration of their cornea histology, which was abolished following supplementation with gallic acid or its combination with glibenclamide. Conclusions: The study showed the potentials of gallic acid and glibenclamide in mitigating systemic complication and histological changes in the cornea of diabetic rats induced with STZ.
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Animales , Ratas , Gliburida/administración & dosificación , Estreptozocina/administración & dosificación , Córnea/efectos de los fármacos , Diabetes Mellitus , Ácido Gálico/administración & dosificaciónRESUMEN
Purpose: Reflux esophagitis is a condition characterized by inflammation and irritation of the esophagus, resulting from the backflow of stomach acid and other gastric contents into the esophagus. Columbianadin is a coumarin derivative that exhibits anti-inflammatory and antioxidant effects. In this study, we tried to scrutinize the protective effect of Columbianadin against acute reflux esophagitis in rats. Methods: RAW 264.7 cells were utilized to assess cell viability and measure the production of inflammatory parameters. The rats received anesthesia, and reflux esophagitis was induced via ligation of pylorus and fore stomach and corpus junction. Rats received the oral administration of Columbianadin (25, 50 and 100 mg/kg) and omeprazole (20 mg/kg). The gastric secretion volume, acidity, and pH were measured. Additionally, the levels of oxidative stress parameters, cytokines, and inflammatory markers were determined. At the end of the study, mRNA expression was assessed. Results: Columbianadin remarkably suppressed the cell viability and production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and prostaglandin (PGE2). Columbianadin treatment remarkably suppressed the secretion of gastric volume, total acidity and enhanced the pH level in the stomach. Columbianadin remarkably altered the level of hydrogen peroxidase, free iron, calcium, and plasma scavenging activity, sulfhydryl group; oxidative stress parameters like malonaldehyde, glutathione, superoxide dismutase, catalase, glutathione peroxidase; inflammatory cytokines viz., TNF-α, IL-6, IL-1ß, IL-10, IL-17, and monocyte chemoattractant protein-1; inflammatory parameters including PGE2, iNOS, COX-2, and nuclear kappa B factor (NF-κB). Columbianadin remarkably (P < 0.001) suppressed the mRNA expression TNF-α, IL-6, IL-1ß and plasminogen activator inhibitor-1. Conclusions: Columbianadin demonstrated a protective effect against acute reflux esophagitis via NF-κB pathway.
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Animales , Ratas , Esofagitis Péptica , Reflujo Gastroesofágico , FN-kappa B , Estrés Oxidativo , InflamaciónRESUMEN
PURPOSE: Diabetes mellitus is a serious health problem worldwide, and diabetic nephropathy is the complication. The diabetic nephropathy considerably enhances the oxidative stress, glycation, lipid parameters and inflammatory reaction. Ellipticine has potent free radical scavenging and anti-inflammatory effect. METHODS: In the current study, our objectives were to thoroughly examine the renal protective effects of ellipticine in a rat model of streptozotocin (STZ)-induced diabetic nephropathy (DN) and to elucidate the underlying mechanisms involved. For the induction of diabetic nephropathy, streptozotocin (50 mg/kg) was used, and rats were separated into groups and given varying doses of ellipticine (2.5, 5 and 7.5 mg/kg). The body weight, and renal weight were estimated. The inflammatory cytokines, renal biomarkers, inflammatory antioxidant, and urine parameters were estimated. RESULTS: Result showed that ellipticine considerably enhanced the body weight and reduced the renal tissue weight. Ellipticine treatment significantly (P < 0.001) repressed the level of blood urea nitrogen, serum creatinine, uric acid, blood glucose and altered the lipid parameters. Ellipticine significantly (P < 0.001) repressed the level of malonaldehyde and boosted the glutathione, catalase, superoxide dismutase, and glutathione peroxidase. Ellipticine treatment significantly (P < 0.001) reduced the inflammatory cytokines and inflammatory mediators. CONCLUSIONS: Ellipticine could be a renal protective drug via attenuating the inflammatory reaction, fibrosis and oxidative stress in streptozotocin induced rats.
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Diabetes Mellitus , Nefropatías Diabéticas , Elipticinas , Ratas , Animales , Nefropatías Diabéticas/tratamiento farmacológico , Nefropatías Diabéticas/prevención & control , Nefropatías Diabéticas/metabolismo , Estreptozocina/metabolismo , Estreptozocina/farmacología , Estreptozocina/uso terapéutico , Elipticinas/metabolismo , Elipticinas/farmacología , Elipticinas/uso terapéutico , Riñón , Estrés Oxidativo , Citocinas/metabolismo , Mediadores de Inflamación/metabolismo , Peso Corporal , Diabetes Mellitus/metabolismoRESUMEN
Acute Lung Injury (ALI) is a critical medical condition that induces the injury into the lung tissue, resulting in decreased the oxygen levels in the circulation and finally causes the respiratory failure. In this study, we try to made effort for scrutinized the preventive effect of gossypin against lipopolysaccharide (LPS) induced lung inflammation and explore the underlying mechanism. LPS (7.5 mg/kg) was used for induction the lung inflammation in the rats and rats were received the oral administration of gossypin (5, 10 and 15 mg/kg). The wet to dry weight lung ratio and lung index were estimated. The bronchoalveolar lavage fluid (BALF) were collected to determination the inflammatory cells, total protein, macrophages and neutrophils. ELISA kits were used for the estimation of antioxidant, inflammatory cytokines, inflammatory parameters, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) parameters. Finally, we used the lung tissue for scrutinize the alteration in the lung histopathology. Gossypin treatment significantly (p < .001) reduced the W/D ratio of lung tissue and lung index. Gossypin significantly (p < .001) decreased the total cells, neutrophils, macrophages and total protein in BALF. It is also altered the level of inflammatory cytokines, antioxidant and inflammatory parameters, respectively. Gossypin improved the level of Nrf2 and HO-1 at dose dependent manner. Gossypin treatment remarkably enhance the ALI severity via balancing the structural integrity of lung tissue, decrease the thickness of the alveolar wall, decline the pulmonary interstitial edema, and number of inflammatory cells in the lung tissue. Gossypin is a promising agent for the treatment of LPS induced lung inflammation via altering Nrf2/HO-1 and NF-κB.
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Lesión Pulmonar Aguda , Neumonía , Ratas , Animales , FN-kappa B/metabolismo , Lipopolisacáridos/toxicidad , Hemo-Oxigenasa 1/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , Antioxidantes/metabolismo , Transducción de Señal , Pulmón , Lesión Pulmonar Aguda/metabolismo , Neumonía/patología , Citocinas/metabolismo , Inflamación/metabolismoRESUMEN
Purpose: Diabetes mellitus is a serious health problem worldwide, and diabetic nephropathy is the complication. The diabetic nephropathy considerably enhances the oxidative stress, glycation, lipid parameters and inflammatory reaction. Ellipticine has potent free radical scavenging and anti-inflammatory effect. Methods: In the current study, our objectives were to thoroughly examine the renal protective effects of ellipticine in a rat model of streptozotocin (STZ)-induced diabetic nephropathy (DN) and to elucidate the underlying mechanisms involved. For the induction of diabetic nephropathy, streptozotocin (50 mg/kg) was used, and rats were separated into groups and given varying doses of ellipticine (2.5, 5 and 7.5 mg/kg). The body weight, and renal weight were estimated. The inflammatory cytokines, renal biomarkers, inflammatory antioxidant, and urine parameters were estimated. Results: Result showed that ellipticine considerably enhanced the body weight and reduced the renal tissue weight. Ellipticine treatment significantly (P < 0.001) repressed the level of blood urea nitrogen, serum creatinine, uric acid, blood glucose and altered the lipid parameters. Ellipticine significantly (P < 0.001) repressed the level of malonaldehyde and boosted the glutathione, catalase, superoxide dismutase, and glutathione peroxidase. Ellipticine treatment significantly (P < 0.001) reduced the inflammatory cytokines and inflammatory mediators. Conclusions: Ellipticine could be a renal protective drug via attenuating the inflammatory reaction, fibrosis and oxidative stress in streptozotocin induced rats.
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Animales , Ratas , Estreptozocina , Estrés Oxidativo , Nefropatías Diabéticas , Elipticinas , Inflamación , AntioxidantesRESUMEN
Objective: Surgical face masks have been recommended by World Health Organization (WHO) during the COVID-19 pandemic. Nowadays wearing masks have become a norm and lifestyle around the globe. The present investigation was carried out to evaluate the feasibility of developing masks loaded with analytical grade sodium chloride (NaCl), Iodized salts (IS) and Omani sea salt (OSS) with or without sodium bicarbonate (NaHCO3). Methods: The saline loaded masks were prepared by soaking the middle layer of the mask in 30% (w/v) saline solutions (NaCl, IS, OSS) with or without 10% NaHCO3 for 24 h followed by drying at room temperature. The prepared saline solutions and its combinations were evaluated for antimicrobial efficacy against the bacteria like Escherichia coli, Pseudomonas aeruginosa, Proteus vulgaris, Salmonella typhi, and Staphylococcus aureus, and antifungal activity against the Penicillium spp. and Rhizopus spp. by agar diffusion. Optical microscopy was employed to observe the formation of salt crystal in the mask material. Survivability of S. aureus and P. aeruginosa was tested on the mask material loaded with 30% OSS + 10% NaHCO3 at particular time intervals. Results: The results showed that a combination of 30% OSS + 10% NaHCO3 exhibited promising antimicrobial activity against all the bacteria as well as Rhizopus spp. compared to the 30% IS + 10% NaHCO3. Moreover, the middle layer of the mask loaded with saline solutions of 30% OSS + 10% NaHCO3 or 30% IS + 10% NaHCO3 have antibacterial activity, particularly for oral microbiome. On dehydration, the masks materials showed the presence of a significant amount of salt crystals. Survivability tests showed that both S. aureus and P. aeruginosa were killed within 3 h of contact with the salt crystals on the mask materials. Conclusions: A combination of 30% OSS + 10% NaHCO3 possessed significant antimicrobial activities on the tested microorganisms. Presence of a significant amount of salt crystals on dehydration of the saline loaded masks can be used as an effective protective barrier to infectious respiratory agents.
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Meloidogyne incognita is an important plant-parasitic nematode that causes significant crop losses all over the world. The primary control strategy for this pathogen is still based on nematicides, which are hazardous to human health and the environment. Considering these problems, this study aimed to determine the efficacy of different concentrations (25, 50, and 100 ppm) of silver nanoparticles against M. incognita on Trachyspermum ammi. Silver nanoparticles synthesized from Senna siamea were thoroughly characterized using various physicochemical techniques, viz., UV-visible spectrophotometer, scanning electron microscopy (SEM), transmission electron microscopy (TEM), and energy-dispersive X-ray analyzer (EDX). Results revealed that plants treated with 50 ppm silver nanoparticles one week before M. incognita inoculation (T2) exhibited maximum and significant (p ≤ 0.05) increases in plant growth, biochemical characteristics, and activities of defense enzymes such as peroxidase, catalase, superoxide dismutase, and ascorbate peroxidase over the inoculated control (IC) plants. Furthermore, the maximum reduction in the number of galls, egg masses, and root-knot indices was recorded in plants treated with 100 ppm silver nanoparticles (T3) followed by plants treated with 50 ppm silver nanoparticles before nematode inoculation (T2), over inoculated plants (IC). Anatomical studies showed accumulation of lignin in the transverse section (TS) of roots treated with 50 ppm silver nanoparticles. As a result, the present finding strongly suggests that silver nanoparticles synthesized from S. siamea had nematicidal activity, and it could be an efficient, safe, cost-effective, and affordable alternative to chemical nematicide.
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The formation of bacterial biofilms is a severely encountered problem in clinical and industrial settings. Most of the naturally occurring bacterial strains are capable of forming mono or mixed biofilms. In this study, we evaluated the potentiality of three clinically relevant species in forming mono and mixed biofilms over glass surface. In addition, we also appraised the efficiency of bacteriophages in alleviating preformed mono and mixed biofilm. Our initial study focused on the ability of Escherichia coli, Staphylococcus aureus, and Pseudomonas aeruginosa in forming biofilm on glass cover slip. All the three strains were able to form mono biofilm, although at varying intensities. Interestingly, E. coli inhibited the formation of S. aureus biofilm in a mixed culture. Specific bacteriophages ɸ44AHJD and ɸX174 completely disrupted S. aureus and E. coli preformed biofilm structure after 72 hr of incubation. However, addition of either of the bacteriophage to the mixed E. coli-S. aureus promoted the formation of biofilm by the alternate strain that was not affected by the phage. Our findings elicit the potentiality of common bacterial strains in forming biofilms on smooth glass surface. In addition, these results are very promising for the development of effective drugs using intact bacteriophages for the removal of complicated bacterial biofilms formed in clinically relevant glass surfaces. The observations further complemented the earlier finding of competitive inhibition of S. aureus biofilm development by E. coli.
Asunto(s)
Bacteriófagos , Escherichia coli , Biopelículas , Pseudomonas aeruginosa , Staphylococcus aureusRESUMEN
Most bacteria exist in nature in the form of biofilms. One of the key survival strategies by bacteria to withstand chemical and physical stresses is by forming biofilms on biotic and abiotic surfaces. A different set of genes are expressed in biofilms compared to the planktonic mode of bacterial growth. According to data from the National Institutes of Health (NIH) and Centers for Disease Control and Prevention (CDC), nearly 80 percent of all human infections are encouraged by biofilms and roughly 65 percent of all hospital-acquired infections are associated with biofilms. Hence, considering the role of biofilms in clinical settings, there is an urgent need for the discovery/development of novel antibiofilm agents. In this study, we have tested the effect of freshly prepared titanium dioxide nanoparticles (TiO2-NPs) synthesized using Carum copticum extract on biofilms, both against Gram +ve and Gram -ve bacteria. Being environment friendly in nature, the green route of nanoparticle synthesis is believed to be advantageous over chemical synthesis of metal nanoparticles. The synthesized nanoparticles were found to be predominantly spherical or spheroidal in shape with an average size of 12.01 ± 5.58 nm. As evident from data, more than 70% inhibition of biofilms of test bacteria was achieved in the presence of TiO2-NPs. Electron microscopic analysis revealed that the adherence and colonization of bacteria on the glass surface were remarkably reduced by the treatment of TiO2-NPs. The EPS secretion of E. coli ATCC 25922 and P. aeruginosa PAO1 were inhibited by 62.08 and 74.94%, respectively. The EPS secretion of S. aureus MTCC 3160 was least inhibited (<55%) compared to other test bacteria. Moreover, TiO2-NPs successfully eradicated the preformed biofilms of E. coli ATCC 25922, P. aeruginosa PAO1, and S. aureus MTCC 3160 by 60.09, 64.14, and 48.30%, respectively. The findings demonstrate the efficacy of green synthesized titanium dioxide nanoparticles in inhibiting and eradicating the biofilms of bacterial pathogens and they may be further exploited for the development of a new alternative antibiofilm agent.
RESUMEN
The effects of tetramethrin and prallethrin exposure on plasma total proteins, free amino acids, albumins, urea, urea nitrogen, uric acid, creatinine were tested. Serum SGOT, SGPT and lipid profile, antioxidants super oxide dismutase (SOD), catalase, GSH, G-Px, phospholipids, cholesterol, C/P ratio in membranes of erythrocyte and membrane fluidity were analyzed. The reason of the study were analyzed to examine the possessions of mosquito repellent pyrethroid (MRP) based compounds tetramethrin and prallethrin exposure on plasma profile, antioxidant status of erythrocyte membrane, membrane fluidity in male Wistar rats. We tested chronically for three months exposure every day (continuously for 8-10 h per day by inhalation) of tetramethrin and prallethrin markedly available (MRP) repellents treated on male Wistar rats. Our results confirmed that tetrarmethrin and prallethrin treatment effect of plasma profile alterations, and lipid homeostasis mechanism in Red Blood cells (RBCs). Tetramethrin and prallethrin treatment significantly increased in erythrocyte membrane phospholipids and decreased levels of cholesterol with no change of protein content, increased C/P ration levels. Inhalation of tetramethrin and prallethrin stimulate plasma biophysical and biochemical modify SGOT, SGPT, erythrocyte membrane cholesterol and phospholipid levels, individual phospholipids and membrane fluidity of exposure rats compared to controls.
RESUMEN
Channa gachua were monthly sampled throughout a year and the histological analysis of their ovaries was done to determine the changes occurring in ovarian development. Based on histological examination of the ovaries, the oogenic process of C. gachua undergoes distinct cyclic and seasonal morphological changes. Five different developmental stages were identified under three major categories: pre-spawning (immature, maturing, mature), spawning (ripe-running) and post-spawning (spent). The peak spawning period of C. gachua was noticed during December - February. The gonadosomatic index (GSI) and ova diameter ranged from 0.79 to 3.61% and 543-1123 µm respectively. The highest mean GSI (3.61 ± 0.16) and oocyte diameter (1123 ± 55 µm) were observed in December indicating that during this month the gonadal development reached maturity.