Publications by authors named "Sureshkumar Anandasadagopan"

In the past few decades, the design and fabrication of bio-scaffolds exhibiting structural stability in long-term and biocompatibility has received much attention in the field of tissue engineering application. In this direction, we have synthesized different mole ratio of PdO-TiO nanocomposites (1:1, 2:1 and 3:1 of Pd:Ti, size 5-11nm, 7-16 nm and 9-22 nm) through a simple single step sol-gel method. The obtained nanocomposites of different sizes were assimilated into poly (methyl methacrylate) grafted collagen biopolymer (g-PMMA-Collagen), resulting in a PdO-TiO-g-PMMA-Collagen based scaffold.

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Chemotherapeutic drugs exert systemic toxicity in lung cancer cells and therefore novel treatment strategies are warranted. Epigallocatechin 3-gallate (EGCG), though possessing beneficial effects in alleviating cancer, its effect has been limited due to ineffective systemic delivery, toxicity and bioavailability. To attain the maximum therapeutic response of EGCG, we have synthesized bovine serum albumin (BSA) encapsulated magnetite nanoparticle (MNPs) loaded with EGCG (nano EGCG).

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Pulmonary fibrosis (PF) is a chronic pulmonary disease of unknown cause with high mortality. Autophagy is an important homeostatic process that decides the fate of cells under stress conditions. This study is aimed to investigate whether impaired autophagic activity leads to fibrosis and pharmacological induction of autophagy provides protection against bleomycin (BLM)-induced PF.

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Pulmonary fibrosis (PF) is characterized by excessive accumulation of extracellular matrix components in the alveolar region which distorts the normal lung architecture and impairs the respiratory function. The aim of this study is to evaluate the anti-fibrotic effect of celastrol, a quinine-methide tri-terpenoid mainly found in Thunder God Vine root extracts against bleomycin (BLM)-induced PF through the enhancement of antioxidant defense system. A single intratracheal instillation of BLM (3 U/kg.

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Alcohol treatment induces oxidative stress by a combination of increased production of partially reduced oxygen species and decreased cellular antioxidant pool, including GSH. Recently, we showed that mitochondrion-targeted CYP2E1 augments alcohol-mediated toxicity, causing an increase in reactive oxygen species production and oxidative stress. Here, we show that cytochrome c oxidase (CcO), the terminal oxidase of the mitochondrial respiratory chain, is a critical target of CYP2E1-mediated alcohol toxicity.

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