http://192.168.1.40:8080/xmlui/handle/123456789/1426 2026-05-31T14:25:02Z http://192.168.1.40:8080/xmlui/handle/123456789/2455 Protective effect of a 43 kD protein from the leaves of the herb, cajanus indicus L on chloroform induced hepatic-disorder Ghosh, A.; Sarkar, K.; Sil, Parames Chandra Cajanus indicus is a herb with medicinal properties and is traditionally used to treat various forms of liver disorders. Present study aimed to evaluate the effect of a 43 kD protein isolated from the leaves of this herb against chloroform induced hepatotoxicity. Male albino mice were intraperitoneally treated with 2 mg/kg body weight of the protein for 5 days followed by oral application of chloroform (0.75 ml/kg body weight) for 2 days. Different biochemical parameters related to physiology and pathophysiology of liver, such as, serum glutamate pyruvate transaminase and alkaline phosphatase were determined in the murine sera under various experimental conditions. Direct antioxidant role of the protein was also determined from its reaction with Diphenyl picryl hydraxyl radical, superoxide radical and hydrogen peroxide. To find out the mode of action of this protein against chloroform induced liver damage, levels of antioxidant enzymes catalase, superoxide dismutase and glutathione-S-transferase were measured from liver homogenates. Peroxidation of membrane lipids both in vivo and in vitro were also measured as malonaldialdehyde. Finally, histopathological analyses were done from liver sections of control, toxin treated and protein pre- and post-treated (along with the toxin) mice. Levels of serum glutamate pyruvate transaminase and alkaline phosphatase, which showed an elevation in chloroform induced hepatic damage, were brought down near to the normal levels with the protein pretreatment. On the contrary, the levels of antioxidant enzymes such as catalase, superoxide dismutase and glutathione-S-transferase that had gone down in mice orally fed with chloroform were significantly elevated in protein pretreated ones. Besides, chloroform induced lipid peroxidation was effectively reduced by protein treatment both in vivo and in vitro. In cell free system the protein effectively quenched diphenyl picryl hydrazyl radical and superoxide radical, though it could not catalyse the breakdown of hydrogen peroxide. Post treatment with the protein for 3 days after 2 days of chloroform administration showed similar results. Histopathological studies indicated that chloroform induced extensive tissue damage was less severe in the mice livers treated with the 43 kD protein prior and post to the toxin administration. Results from all these data suggest that the protein possesses both preventive and curative role against chloroform induced hepatotoxicity and probably acts by an anti-oxidative defense mechanism. 2006-03-31T00:00:00Z http://192.168.1.40:8080/xmlui/handle/123456789/2451 Curative role of the aqueous extract of the herb, Phyllanthus niruri, against nimesulide induced oxidative stress in murine liver Sarkar, M.K.; Sarkar, K.; Bhattacharjee, R.; Chatterjee, M.; Sil, Parames Chandra The present study was conducted to evaluate whether the aqueous extract of the herb, Phyllanthus niruri (PN) can effectively cure liver from nimesulide (NIM) induced oxidative stress in vivo. In our experiments, we have seen that administration of PN through intraperitoneal route is more effective in hepato-protection than oral administration. PN (100 mg/kg body weight) was, therefore, administered intraperitoneally for 5 days post to NIM application (10 mg/kg body weight/twice daily) for 7 days in mice. Levels of antioxidant enzymes like superoxide dismutase (SOD) and catalase (CAT), non-protein thiol reduced glutathione (GSH) and lipid peroxidation end-products were then determined. NIM administration caused significant depletion of the levels of SOD, CAT and GSH along with the increased levels of lipid peroxidation. Post-treatment with PN rapidly restored most of the NIM-induced oxidative changes compared to those obtained by the self recovery of liver. Histological studies supported these results. In addition, studies showed that PN could scavenge free radicals. Antioxidant property of PN has been compared with that of potent antioxidant, vitamin E. Besides, the effect of a non-relevant protein, BSA, has also been included in the study. Combining, data suggest that NIM induced oxidative stress in the liver and that could be cured by the beneficial effect of PN. 2005-10-01T00:00:00Z http://192.168.1.40:8080/xmlui/handle/123456789/2449 Characterization and functional significance of myotrophin: A gene with multiple transcripts Adhikary, G.; Gupta, S.; Sil, Parames Chandra; Saad, Y.; Sen, S. The underlying mechanism for the development of cardiac hypertrophy that advances to heart failure is not known. Many factors have been implied to play a role in this process. Among others, we have isolated and identified myotrophin, a factor that stimulates myocytes growth, from spontaneously hypertensive rat (SHR) heart and patients with dilated cardiomyopathy. The gene encoding myotrophin has been cloned and expressed in E. coli. Recently, myotrophin gene has been mapped and shown to be a novel gene localized in human chromosome 7q-33. To define the characteristics of each transcript and its pathophysiological significance, we examined transcripts of myotrophin in SHR heart during progression of hypertrophy. Northern blot analysis of myotrophin mRNA showed multiple transcripts. We isolated and characterized various myotrophin cDNA clones corresponding to the multiple transcripts by 5' "stretch plus" rat heart cDNA library screening. Sequence analysis of these cDNA clones indicates that each clone has a unique 5' UTR and multiple 3' UTR with varying lengths, repeated ATTTA motifs and many polyadenylation signals. In vitro transcripts generated from all these myotrophin-specific cDNA clones translate in vitro to a 12-kD protein. Among pathophysiological significance, we determined mRNA expression in 9 days old, 3 weeks old and 31 weeks old and observed a linear increased during the progression of hypertrophy. In WKY, this mRNA level remained the same throughout the growth and development of hypertrophy. Our data strongly suggest that myotrophin appears to be a candidate gene for cardiac hypertrophy and heart failure. DOI: 10.1016/j.gene.2005..03.045 2005-06-20T00:00:00Z http://192.168.1.40:8080/xmlui/handle/123456789/2447 Preventive and curative role of a 43 kD protein from the leaves of the herb Cajanus indicus L on thioacetamide-induced hepatotoxicity in vivo Sarkar, K; Ghosh, A.; Sil, Parames Chandra An approximately 43 kD protein has been isolated and purified from the herb Cajanus indicits L and believed to be the most active principle for its hepatoprotective action. In this study, experiments have been performed to evaluate the effectiveness of that protein for the preventive and curative action against thioacetamide-induced toxicity in vivo using a murine model. Mice were treated with the protein intraperitoneally at a dose of 2 mg/kg body weight for 2 and 6 days before and separately 1-5 days after thioacetamide administration to evaluate its preventive and curative role, respectively. Thioacetamide was administered once at a dose of 150 mg/kg body weight and after 48 h of its application, the animals were sacrificed. Levels of various markers related to physiological and pathological conditions of the liver, e.g., glutamate pyruvate transaminase (GPT), alkaline phosphatase (ALP), etc. were determined in the, murine sera under different experimental conditions. In addition, antioxidant enzymes glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) as well as thiobarbituric acid reactive substances (TBARS), were measured from the liver homogenates. The antioxidant property of the protein was compared with the potent antioxidant, vitamin E (used as a positive control). The active principle effectively reduced the elevated GPT and ALP levels in serum and lipid peroxidation in the liver tissue. The reduced levels of SOD, CAT and GST by thioacetamide were again brought back to almost normal levels upon pre- and post-treatment with the protein. Histopathological changes in the liver of TAA control and protein-treated groups also prove that the protein possesses hepatoprotective activity. The protein acts dose-dependently and maximum hepatoprotectivity was obtained when administered at a dose of 2 mg/kg body weight. Data suggest that the active principle plays an important preventive and curative role against thioacetamide-induced hepatotoxicity. DOI: 10.1016/j.hepres.2005.06.007 2005-09-01T00:00:00Z