8 results on '"Velayutham, Ravichandiran"'
Search Results
2. Glucogallin Attenuates RAW 264.7 Cells from Arsenic Trioxide Induced Toxicity via the NF-ҡB/NLRP3 Pathway
- Author
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Anam Najib Khan, Rajveer Singh, Arka Bhattacharya, Sonu Kumar, Arijit Ghosh, Debasish Nag, Velayutham Ravichandiran, and Dipanjan Ghosh
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Organic Chemistry ,NF-kappa B ,Pharmaceutical Science ,Apoptosis ,Oxides ,Hydrolyzable Tannins ,Arsenic ,Analytical Chemistry ,Mice ,Oxidative Stress ,RAW 264.7 Cells ,Arsenic Trioxide ,Chemistry (miscellaneous) ,Arsenic Poisoning ,NLR Family, Pyrin Domain-Containing 3 Protein ,Drug Discovery ,Animals ,Molecular Medicine ,Physical and Theoretical Chemistry ,Reactive Oxygen Species - Abstract
Chronic arsenic (As) poisoning is mostly due to subsoil water contaminated with As and its salts. Exposure to As has been found to cause an elevation in reactive oxygen species (ROS), leading to the damage of DNA and proteins, and it also causes immunotoxicity. Treatment regimens are primarily based on chelation therapy and amino acid and vitamin supplementations. Recent studies have established that natural products display effective and progressive relief from arsenicosis without any side effects. β-glucogallin (BGG), a gallo-tannin natural product, is reported to possess anti-oxidant and anti-inflammatory properties. In the present study, we aim to observe the protective role of BGG against As-induced cytotoxicity, apoptosis, mitochondrial dysfunction, and the underlying mechanisms in RAW 264.7 macrophage cells. We found that BGG alleviates As-induced ROS, apoptosis, and mitochondrial dysfunction in RAW 264.7 macrophage cells. Thus, BGG can be used therapeutically to prevent As-induced toxicity.
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- 2022
3. Melatonin prevents diabetes‐induced nephropathy by modulating the AMPK/SIRT1 axis: Focus on autophagy and mitochondrial dysfunction.
- Author
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Siddhi, Jain, Sherkhane, Bhoomika, Kalavala, Anil Kumar, Arruri, Vijay, Velayutham, Ravichandiran, and Kumar, Ashutosh
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DIABETIC nephropathies ,NUCLEAR factor E2 related factor - Abstract
Impaired nutrient sensing mechanisms such as AMPK/silent information regulator type 1 (SIRT1) axis and autophagy in renal cells upon chronic diabetic condition accelerate renal injury and upregulating these mechanisms has been reported to prevent renal damage. Melatonin, a neuroendocrine agent, also possess antioxidant and AMPK modulatory effect. In the current study, the protective effect of melatonin against diabetic renal injury was assessed in streptozotocin‐induced diabetic nephropathy model and in in vitro model of high‐glucose‐induced tubular injury. Melatonin (3 and 10 mg/kg) was administered for 28 days after 4 weeks of diabetes induction in Sprague–Dawley rats. For in vitro model, the NRK‐52E cells were co‐incubated with high glucose and melatonin (25 and 50 μM). Melatonin supplementation abrogated the diabetes‐induced renal injury and improved renal function in diabetic rats. Immunoblot analysis of renal tissue lysates revealed improved expression of AMPK, as well as upregulated the expression of nuclear factor erythroid 2‐related factor 2, SIRT1, PGC‐1α, TFAM and enhanced autophagy upon melatonin treatment in diabetic rats. Likewise, melatonin treatment in high glucose exposed NRK‐52E cells improved expression of AMPK, enhanced mitochondrial biogenesis and positively modulated autophagy. However, these effects were repressed upon inhibition of AMPK activity in NRK‐52E cells by treatment of Compound‐C, suggesting that the protective effects of melatonin were mainly mediated through activation of AMPK. These results suggest that melatonin might mediate the renoprotective effect by upregulating the AMPK/SIRT1 axis, enhancing the autophagy and mitochondrial health in DIabetic Nephropathy. Highlights: 1.Melatonin improves renal function in streptozotocin‐induced diabetic nephropathy model.2.Melatonin upregulates AMPK/SIRT1 axis, mitochondrial biogenesis and autophagy in diabetic kidney and in high‐glucose‐exposed NRK‐52E cells.3.Inhibition of AMPK prevents protective effect of melatonin in NRK‐52E cells. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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4. Survival upon Staphylococcus aureus mediated wound infection in Caenorhabditis elegans and the mechanism entailed
- Author
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Krishnan Venkateswaran, Bhaskar J. Prabhanand, Das Shibendu Sekhar, Velayutham Ravichandiran, Krishnaswamy Balamurugan, Kanagavel Suruthi, Murali Deepa, Gajbhiye Rahul, and Murugesan Pooranachithra
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Proteomics ,0301 basic medicine ,MAPK/ERK pathway ,Staphylococcus aureus ,030106 microbiology ,Mutant ,Oxidative phosphorylation ,medicine.disease_cause ,Microbiology ,03 medical and health sciences ,Wound care ,chemistry.chemical_compound ,medicine ,Animals ,Phosphatidylinositol ,Caenorhabditis elegans ,Caenorhabditis elegans Proteins ,Pathogen ,integumentary system ,biology ,Hydrogen Peroxide ,biology.organism_classification ,Oxidative Stress ,030104 developmental biology ,Infectious Diseases ,chemistry ,Wound Infection - Abstract
Infection following injury is one of the major threats which causes huge economic burden in wound care management all over the world. Injury often results with poor healing when coupled by following infection. In contrast to this, we observed enhanced survival of wound infected worms compared to wounded worms in Caenorhabditis elegans wound model while infecting with Staphylococcus aureus. Hence, the study was intended to identify the mechanism for the enhanced survival of wound infected worms through LCMS/MS based high throughput proteomic analysis. Bioinformatics analyses of the identified protein players indicated differential enrichment of several pathways including MAPK signaling, oxidative phosphorylation and phosphatidylinositol signaling. Inhibition of oxidative phosphorylation and phosphatidylinositol signaling through chemical treatment showed complete reversal of the enhanced survival during wound infection nevertheless mutant of MAPK pathway did not reverse the same. Consequently, it was delineated that oxidative phosphorylation and phosphatidylinositol signaling are crucial for the survival. In this regard, elevated calcium signals and ROS including O- and H2O2 were observed in wounded and wound infected worms. Consequently, it was insinuated that presence of pathogen stress could have incited survival in wound infected worms with the aid of elevated ROS and calcium signals.
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- 2021
5. Influence of alpha lipoic acid on antioxidant status in D-galactosamine-induced hepatic injury
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D. Sivaraman, E. Krishnakumar, T.S. Shanmugarajan, R Balaji, M. Arunsundar, I. Somasundaram, and Velayutham Ravichandiran
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Male ,medicine.medical_specialty ,Antioxidant ,Health, Toxicology and Mutagenesis ,medicine.medical_treatment ,Glutathione reductase ,Galactosamine ,Toxicology ,medicine.disease_cause ,Antioxidants ,Transaminase ,Lipid peroxidation ,chemistry.chemical_compound ,Internal medicine ,medicine ,Animals ,Rats, Wistar ,chemistry.chemical_classification ,Analysis of Variance ,Glutathione Peroxidase ,Thioctic Acid ,biology ,Superoxide Dismutase ,Chemistry ,Liver Diseases ,Glutathione peroxidase ,Public Health, Environmental and Occupational Health ,Glutathione ,Catalase ,Rats ,Disease Models, Animal ,Oxidative Stress ,Endocrinology ,Liver ,Alanine transaminase ,Biochemistry ,biology.protein ,Lipid Peroxidation ,Chemical and Drug Induced Liver Injury ,Biomarkers ,Injections, Intraperitoneal ,Oxidative stress - Abstract
D-Galactosamine (GalN)-induced liver injury is associated with reactive oxygen species and oxidative stress. In the present study, we evaluated the effect of alpha lipoic acid (ALA) supplementation on acute GalN-induced oxidative liver injury. Hepatotoxicity induced by single intraperitoneal injection of GalN (500 mg/kg body wt) was evident from increase in lipid peroxidation and serum marker enzymes (asparate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase). The decreased activities of enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) as well as glutathione levels were the salient features observed in GalN-induced hepatotoxicity. Pretreatment with ALA (50 mg/kg body weight for 7 days) significantly precluded these changes and prevents the hepatic injury. Hence, this study clearly exemplified that ALA might be a suitable candidate against GalN-induced cellular abnormalities.
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- 2008
6. Mitigation of azathioprine-induced oxidative hepatic injury by the flavonoid quercetin in wistar rats
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N. Prithwish, M. Niladri, I. Somasundaram, Velayutham Ravichandiran, M. Arunsundar, J P Lavande, and T.S. Shanmugarajan
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chemistry.chemical_classification ,biology ,Health, Toxicology and Mutagenesis ,Glutathione peroxidase ,Glutathione reductase ,Aspartate transaminase ,Glutathione ,Pharmacology ,Toxicology ,Malondialdehyde ,medicine.disease_cause ,Lipid peroxidation ,chemistry.chemical_compound ,Biochemistry ,chemistry ,Alanine transaminase ,medicine ,biology.protein ,Oxidative stress - Abstract
Azathioprine (AZA), one of the widely prescribed immunosuppressant drugs in organ transplantation and autoimmune diseases, could cause hepatotoxicity in the course of therapy. The current work was designed to assess the protective role of the dietary flavonoid, quercetin (QE), in oxidative hepatic damage induced by AZA. Adult male Wistar rats were divided into four treatment groups. Two groups were treated with single intraperitoneal injection of AZA (50 mg/kg body weight); one of these groups was pretreated with QE (50 mg/kg body weight) intraperitoneally once a day for 7 days. A vehicle treated control group and a QE control group were also included. Hepatotoxicity, evident from increased levels of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma glutamyl transpeptidase (GGT) in serum 24 h after AZA treatment, was significantly (p < 0.05) normalized by QE pretreatment. AZA administered rats displayed declined levels of endogenous antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)], along with elevated levels of malondialdehyde (MDA). However, pretreatment with QE significantly precluded lipid peroxidation and maintained the activities of antioxidant defenses at a near normal status. Besides, AZA induced oxidative stress and subsequent DNA damage was effectively manifested by QE, which was confirmed by agarose gel electrophoresis. These findings highlight the salubrious effect of QE as a hepatoprotectant in AZA-induced oxidative stress mediated hepatic injury.
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- 2009
7. Indigenous wisdom of a Kwatha to treat NASH: An insight into the mechanism.
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Yellurkar, Manoj Limbraj, Prasanna, Vani Sai, Das, Pamelika, Sarkar, Sulogna, Matta, Rakesh, Dhaked, Devendra Kumar, Peraman, Ramalingam, Taraphdar, Amit Kumar, Nanjappan, Satheesh Kumar, Velayutham, Ravichandiran, and Arumugam, Somasundaram
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NON-alcoholic fatty liver disease , *COMPUTER-assisted molecular modeling , *IN vitro studies , *INSULIN sensitivity , *HYPERLIPIDEMIA , *PHARMACEUTICAL chemistry , *AYURVEDIC medicine , *OXIDATIVE stress , *HEPATOCELLULAR carcinoma - Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common severe liver disease globally, progressing further into nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC). Vasaguduchyadi Kwatha (VK) is an Ayurvedic formulation traditionally used to treat liver diseases and other metabolic complications. This study is an ethnopharmacological approach to unravel this indigenous remedy. We aimed to discover the probable mechanism of action of VK against NASH in this study, using network pharmacology, molecular docking, in vitro study, and preclinical investigation. Among the 55 components identified, 10 were confirmed based on mass, elution charecteristics, MS/MS analysis data, and fragmentation rules. Computational study indicated 92 targets involved in the central pathways of NASH, out of which only 15 targets and 9 VK constituents have significant docking scores. In vitro and in vivo analysis results showed that VK significantly reduces weight gain and improves insulin sensitivity, dyslipidemia, steatohepatitis and overall histological features of NASH compared to saroglitazar (SGZR). Our detailed study yielded three signalling pathways related to NASH on which VK has maximum effect, bringing up a probable alternative treatment for NASH. [Display omitted] • Imbalance in lipid metabolism, inflammation and oxidative stress foster NASH progression. • Vasaguduchyadi Kwatha, traditionally used to treat liver ailments. • This formulation improved insulin sensitivity, dyslipidaemia and steatohepatitis. • Combination of network pharmacology and systems biology ushers in new targets. [ABSTRACT FROM AUTHOR]
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- 2024
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8. Basidiomycetes-X, an edible mushroom, alleviates the development of atopic dermatitis in NC/Nga mouse model.
- Author
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Watanabe, Kenichi, Karuppagounder, Vengadeshprabhu, Sreedhar, Remya, Kandasamy, Geetha, Harima, Meilei, Velayutham, Ravichandiran, and Arumugam, Somasundaram
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ATOPIC dermatitis , *BASIDIOMYCETES , *EDIBLE mushrooms , *ANTI-inflammatory agents , *OXIDATIVE stress , *LABORATORY mice - Abstract
Abstract Basidiomycetes-X (BDM-X) is a novel edible mushroom recently identified as a new fungi species and is effective against oxidative stress and anti-inflammation associated with immune response. However the effect of BDM-X on atopic dermatitis (AD) has not been elucidated. In this study, we have investigated the effect of BDM-X on AD skin lesions in NC/Nga mouse model. AD-like lesion was induced by the application of house dust mite extract (DfE) to the dorsal skin of NC/Nga mouse. After AD induction, BDM-X was administered once daily for 2 weeks. We have analyzed the effects of BDM-X on dermatitis severity, histopathological changes and changes in inflammatory and proinflammatory proteins expressions in DfE induced AD mice skin. Treatment with BDM-X attenuated the development of AD-like clinical symptoms and effectively inhibited hyperkeratosis, parakeratosis, acanthosis and mast cells in AD mice skin. Furthermore, BDM-X treatment inhibited DfE induced tumor necrosis factor (TNF)α, high mobility group protein (HMG)B1, nuclear factor kappa (NFκ)B and inflammatory cytokines. These results indicate that BDM-X inhibits AD through modulating Th1 and Th2 responses and diminishing the mast cells infiltration in the skin lesions in NC/Nga mice. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
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