ABSTRACT
The present study was designed to investigate the immunomodulatory activity of the ethanolic extract of Tinospora cordifolia [Family: Menispermaceae] stem [climbing shrub, mango plant] at cellular level. For antioxidant study, the liver mitochondria were separated and the concentration of enzymes like lipid peroxidation [LPO], reduced glutathione [GSH], catalase [CAT] and superoxide Dismutase [SOD] were estimated; melatonin secretion characterization was carried out through SDS-PAGE. The spleen lymphocyte proliferation assay was performed through measuring its optical density at 570 nm using Elisa Reader. The cytokines viz. IL-2, IL-10 and TNF-a expression in spleen cells were determined through Real Time PCR. Tinospora cordifolia [Tc] ethanolic extract [100 mg/Kg/p.o.] increased the level of liver mitochondrial enzymes like GSH, CAT and SOD but decreased the level of LPO in liver as compared to the vehicle, SRBC and cyclophosphamide-treated groups. The secretion of melatonin via pineal gland was enhanced with Tc treatment. The extract also increased the spleen lymphocyte proliferation. In RT-PCR analysis, the expression of cytokines viz. IL-2, IL-10 and TNF-alpha was more in Tc-treated animals than vehicle and cyclophosphamide treatment. Hence, the study confirms the immunomodulatory activity of Tc stem through altering the concentration of antioxidant enzymes, increasing T and B cells and antibody which play an important role in immunity, enhancing the concentration of melatonin in pineal gland and increasing the level of cytokines like IL-2, IL-10 and TNF-a which plays an important role in immunity
ABSTRACT
To study the effect of L-arginine on apoptosis and necrosis induced by 1-hischemia followed by 3-h reperfusion. Adult Wistar rats underwent 60 min of partial liver ischemia followed by 3-h reperfusion. Eighteen Wistar rats were divided into sham-operated control group [I] [n = 6], ischemia and reperfusion [I/R] group [0.9% saline [5 mL/kg, orally] for 7 days] [II] [n = 6], and L-arginine-treated group [10 mg/kg body weight daily orally for 7 days before inducing ischemia-reperfusion maneuver] [III] [n = 6]. Apoptotic and necrotic hepatocytes, nitric oxide levels in hepatocytes, Bc1-2 mRNA, and Bc1-2 protein were measured. Liver injury was assessed by plasma alanine transaminases [ALT], aspartate transaminases [AST], liver histopathology, and electron microscopy. An ischemic and reperfusion hepatocellular injury occurred as was indicated by increased serum ALT, AST, histopathology, and electron microscopy. Apoptosis and necrosis associated marker gene Bc1-2 mRNA and protein expression were decreased in I/R group. Pretreatment with L-arginine significantly decreased serum ALT and AST level and apoptotic and necrotic cells after 1 h ischemia followed by 3 h of reperfusion. Nitric oxide production in hepatocytes was increased twofold by L-arginine treatment when compared with 1/ R group. Histopathology and transmission electron microscopy [TEM] studies showed markedly diminished hepatocellular injury in L-argmnine-pretreated rats during the hepatic I/R. Thus, it may be concluded that L-arginine afforded significant protection from necrosis and apoptosis in I/R injury by upregulated Bc1-2 gene and nitric oxide production