Protective Effect of Ginsenoside Against Acute Renal Failure via Reduction of Renal Oxidative Stress and Enhanced Expression of ChAT in the Proximal Convoluted Tubule and ERK1/2 in the Paraventricular Nuclei

Generation of reactive oxygen species significantly contributes to the pathogenesis of acute renal failure (ARF) induced by myoglobin release. Ginsenosides (GS), the principal active ingredients of ginseng, is considered as an extremely good antioxidative composition of Chinese traditional and herbal drugs. The purpose of the present study was to investigate the protective effect of ginsenoside in rats with ARF on the changes of cholinergic nervous system in the kidney as well as on the involvement of mitogen-activated protein kinases (MAPK) in the hypothalamic paraventricular nuclei (PVN). In our assay, glycerol-induced acute renal failure in rats was employed to study the protective effects of ginsenoside. Our results indicated that the treatment of ARF rats with ginsenosides for 48 h significantly reduced lipid peroxidation, restored the superoxide dismutase (SOD) level. Meanwhile, the obvious increase of choline acetyltransferase-immunoreactivity (ChAT-IR) in the proximal convoluted tubular cells (PCT) was observed by immunohistochemistry in ARF+GS group. The same effect was also observed in the changes of p-ERK1/2-IR in the hypothalamic paraventricular nuclei. Our results suggest that ginsenoside administered orally may have a strong renal protective effect against glycerol-induced ARF, reduce the renal oxidative stress, and ginsenoside can also activate the cholinergic system in PCT, simultaneously MAPK signal pathway in the PVN was also activated.

Lesions of hypothalamic paraventricular nuclei do not prevent the effect of estradiol on energy and fat balance

The chronic effects of estradiol (E2) on energy balance have been investigated in ovariectomized rats with hypothalamic paraventricular nuclei (PVH) lesions. Body weight and food intake were monitored throughout the E2 treatment, which lasted 26 days. At the end of this treatment, rats were decapitated, and their carcasses were processed to determine the body contents in energy, fat, and protein. Plasma adrenocorticotropic hormone (ACTH) and corticosterone were determined by radioimmunoassay and protein-binding assay at the end of the study. Regardless of whether they were sham- or PVH-lesioned, E2-treated rats ate, expended, and gained significantly less energy than untreated animals. In addition, E2-treated rats deposited less fat and protein than the rats not receiving E2. In contrast to the E2 treatment, PVH lesions accelerated the gains in energy and fat regardless of whether the rats were treated with E2 or with a placebo. There were no interaction effects of PVH lesions and the E2 treatment on energy or fat gains. Plasma levels of corticosterone and ACTH were higher in E2-treated rats than in animals receiving the placebo treatment. The present results provide evidence that the hypothalamic PVH is not an essential neuroanatomical structure in the effects of E2 on energy and fat balances.