Institution
Central Drug Research Institute
Facility•Lucknow, Uttar Pradesh, India•
About: Central Drug Research Institute is a facility organization based out in Lucknow, Uttar Pradesh, India. It is known for research contribution in the topics: Catalysis & Leishmania donovani. The organization has 4357 authors who have published 7257 publications receiving 143871 citations. The organization is also known as: Central Drug Research Institute, Lucknow & CDRI.
Topics: Catalysis, Leishmania donovani, Ring (chemistry), Aryl, Apoptosis
Papers published on a yearly basis
Papers
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TL;DR: Results indicated that daily administration of antioxidative peptide PEP prevents body weight gain, uterine weight loss, and atrophy of endometrial lumen and demonstrated that PEP exhibits antiosteopenic effects via enhancement of antioxidant activity and reduction of bone-resorbing cytokines expression.
48 citations
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TL;DR: The study shows the beneficial effects of intranasal insulin against STZ‐induced memory impairment, which attributed to improved CBF, cholinergic function, brain energy metabolism, BDNF, Nrf‐2 expression and antioxidative action.
48 citations
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TL;DR: Intracellular calcium rather than oxidative stress is a major factor for rotenone-induced apoptosis in neuronal cells, and melatonin was found ineffective to counteract roten one-induced increased PI uptake, altered morphological changes, DNA damage, elevated Ca+2, and increased expression of caspase-3 and CaMKIIα.
Abstract: Rotenone causes cytotoxicity in astrocytic cell culture by glial activation, which is linked to free radical generation. The present study is an investigation to explore whether rotenone could also cause cellular toxicity in mouse neuroblastoma cells (Neuro-2a) under treatment similar to astroglial cells. The effect of rotenone (0.1, 1, and 10 μM) on mitochondrial dehydrogenase enzyme activity by MTT reduction assay, PI uptake, total reactive oxygen species (ROS)/superoxide levels, nitrite levels, extent of DNA damage (by comet assay), and nuclear morphological alteration by Hoechst staining was studied. Caspase-3 and Ca⁺²/calmodulin-dependent protein kinase II (CaMKIIα) gene expression was determined to evaluate the apoptotic cell death and calcium kinase, respectively. Calcium level was estimated fluorometrically using fura-2A stain. Rotenone decreased mitochondrial dehydrogenase enzyme activity and generated ROS, superoxide, and nitrite. Rotenone treatment impaired cell intactness and nuclear morphology as depicted by PI uptake and chromosomal condensation of Neuro-2a cells, respectively. In addition, rotenone resulted in increased intracellular Ca⁺² level, caspase-3, and CaMKIIα expression. Furthermore, co-exposure of melatonin (300 μM), an antioxidant to cell culture, significantly suppressed the rotenone-induced decreased mitochondrial dehydrogenase enzyme activity, elevated ROS and RNS. However, melatonin was found ineffective to counteract rotenone-induced increased PI uptake, altered morphological changes, DNA damage, elevated Ca⁺², and increased expression of caspase-3 and CaMKIIα. The study indicates that intracellular calcium rather than oxidative stress is a major factor for rotenone-induced apoptosis in neuronal cells.
48 citations
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TL;DR: The findings suggest that FNT inhibits adipogenesis through AMPK/β-catenin signal transduction pathways and protects against HFD-induced obesity and bone loss.
Abstract: Balance between adipocyte and osteoblast differentiation is the key link of disease progression in obesity and osteoporosis. We have previously reported that formononetin (FNT), an isoflavone extracted from Butea monosperma, stimulates osteoblast formation and protects against postmenopausal bone loss. The inverse relationship between osteoblasts and adipocytes prompted us to analyse the effect of FNT on adipogenesis and in vivo bone loss, triggered by high-fat diet (HFD)-induced obesity. The anti-obesity effect and mechanism of action of FNT was determined in 3T3-L1 cells and HFD-induced obese male mice. Our findings show that FNT suppresses the adipogenic differentiation of 3T3-L1 fibroblasts, through down-regulation of key adipogenic markers such as PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα) and sterol regulatory element-binding protein (SREBP) and inhibits intracellular TAG accumulation. Increased intracellular reactive oxygen species levels and AMP-activated protein kinase (AMPK) activation accompanied by stabilisation of β-catenin were attributed to the anti-adipogenic action of FNT. In vivo, 12 weeks of FNT treatment inhibited the development of obesity in mice by attenuating HFD-induced body weight gain and visceral fat accumulation. The anti-obesity effect of FNT results from increased energy expenditure. FNT also protects against HFD-induced dyslipidaemia and rescues deterioration of trabecular bone volume by increasing bone formation and decreasing bone resorbtion caused by HFD. FNT’s rescuing action against obesity-induced osteoporosis commenced at the level of progenitors, as bone marrow progenitor cells, obtained from the HFD mice group supplemented with FNT, showed increased osteogenic and decreased adipogenic potentials. Our findings suggest that FNT inhibits adipogenesis through AMPK/β-catenin signal transduction pathways and protects against HFD-induced obesity and bone loss.
48 citations
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TL;DR: A novel strategy for the Pictet-Spengler reaction is reported that involves reaction of arylamines, linked to the N-1 of disubstituted imidazoles, with aldehydes in the presence of p-TsOH to furnish triazabenzoazulenes as a novel heterosystem.
Abstract: A novel strategy for the Pictet-Spengler reaction is reported. Our strategy involves reaction of arylamines, linked to the N-1 of disubstituted imidazoles, with aldehydes in the presence of p-TsOH. The iminium ion generated in situ undergoes C-C bond formation with the C-5 of the imidazoles to furnish triazabenzoazulenes as a novel heterosystem. Our strategy differs from conventional Pictet-Spengler reaction since the latter utilizes only aliphatic amines in which the amine functionality is linked to a C instead of N of the activated aromatic moiety.
48 citations
Authors
Showing all 4385 results
Name | H-index | Papers | Citations |
---|---|---|---|
Sanjay Kumar | 120 | 2052 | 82620 |
John A. Katzenellenbogen | 95 | 691 | 36132 |
Brajesh K. Singh | 83 | 401 | 24101 |
Gaurav Sharma | 82 | 1244 | 31482 |
Sudhir Kumar | 82 | 524 | 216349 |
Pramod K. Srivastava | 79 | 390 | 27330 |
Mohan K. Raizada | 75 | 473 | 21452 |
Syed F. Ali | 71 | 446 | 18669 |
Ravi Shankar | 66 | 672 | 19326 |
Ramesh Chandra | 66 | 620 | 16293 |
Manoj Kumar | 65 | 408 | 16838 |
Manish Kumar | 61 | 1425 | 21762 |
Anil Kumar Saxena | 58 | 310 | 10107 |
Sanjay Krishna | 56 | 624 | 13731 |
Naibedya Chattopadhyay | 56 | 242 | 9795 |