Anti-GST tag antibody [SureLight® P3]

The objective of the present study was to investigate the hepatoprotective effects of methanol extract of Meconopsis aculeata, an important medicinal plant of Kashmir Himalayas, against CCl4 induced oxidative damage in rats. Acute hepatotoxicity was induced in Wistar albino rats by single intraperitoneal injection of CCl4 at 1 ml/kg body weight dose. Methanol extract of M. aculeata was orally administered at the doses of 100, 200 and 300 mg/kg body weight/day for 14 days. The results revealed that administration of CCl4 caused a significant increase in serum AST, ALT and LDH levels as compared to the control group (p < 0.001). Additionally, there was a significant decrease in the level of hepatic GSH, GPx, GST, SOD and CAT activities associated with a significant increase of MDA content in CCl4 treated group compared to those of the control group. However, the treatment with methanol extract of M. aculeata prevented these alterations and maintained the antioxidant status. The hepatoprotective property of the extract was further confirmed by histopathological analysis, wherein the extract was shown to prevent neutrophil infiltration and tissue necrosis in the liver samples of treated animals. The results of the present investigation indicate that methanol extract of M. aculeata possesses potent hepatoprotective activity, possibly due to its antioxidant properties.

Unpredictable chronic mild stress (UCMS) has been shown to cause memory loss via increased oxidative stress and deregulation of monoaminergic and cholinergic neurotransmissions. Although the benefits of methyl jasmonate (MJ), a well-known anti-stress plant hormone against chronic stress-induced psychopathologies, have been earlier reported, its effects on antioxidant defense molecules, monoaminergic transmitters, and nuclear factor erythroid 2-related factor 2 (Nrf2) immunopositive cells have not been extensively studied. The present study was designed to examine its effect on memory functions, antioxidant biomarkers, monoaminergic transmitters, and Nrf2 immunopositive cell expression in rats exposed to UCMS. Rats received an intraperitoneal injection of MJ (10, 25, and 50 mg/kg) 30 min before exposure to UCMS daily for 28 days. Memory function was assessed on day 29 using a modified elevated plus maze and novel object recognition tests. The antioxidant biomarkers, level of monoamines (serotonin, noradrenaline, and dopamine), and Nrf2 immunopositive cell expression were determined in the rat brain tissues. The activity of cholinesterase and monoamine oxidase enzymes was also determined. MJ attenuated memory deficits and elevated the brain levels of monoamines in UCMS rats. UCMS-induced increase of brain cholinesterase and monoamine oxidase activities was inhibited by MJ. Also, MJ attenuated UCMS-induced decrease in antioxidant enzymes (CAT, GPx, GST, and SOD) and thiol contents in the brains of rats. UCMS-induced increase in NO level and Nrf2 immunopositive cell expression in the rat's brain was attenuated by MJ. Taken together, these findings suggest that increasing antioxidant defense molecules and monoaminergic/cholinergic neurotransmitters and decreasing the Nrf2 immunopositive cell expressions may contribute to the memory-promoting effects of MJ in rats exposed to UCMS.