Protective effect and mechanism of Schisandra chinensis extract on oxidative stress in diabetic nephropathy mice / 中草药

ABSTRACT

Objective: To investigate the protective effect of Schisandra chinensis extract on oxidative stress in db/db mice, and to explore its possible mechanism. Methods: Ten male 9-week-old db/m mice and ten homologous male db/db mice of the same age were randomly divided into normal control group (C + V group), S. chinensis extract control group (C + SE group), model group (DN + V group), and S. chinensis extract-treated group (DN + SE group), with five mice in each group. The S. chinensis extract control group and S. chinensis extract-treated group were respectively ig administrated with 5 mg/(kg•d) of S. chinensis extract for 6 weeks. The body weight, blood glucose and 24 h urine micro-albumin were recorded at 0, 3, and 6 weeks. After 6 weeks, the mice were sacrificed and their kidney tissue specimens were collected. The oxidative stress index of malondialdehyde (MDA) were examined by lipid peroxidation kit. The pathological changes of kidney tissues were observed by PAS staining. The expression of antioxidant factor Nrf2 and HO-1 protein of kidney tissue was detected by Western Blotting. The expression of Nrf2 and its downstream target genes of kidney tissue were detected by qRT-PCR. Results: Compared with the normal control group, the body weight, blood glucose and 24h urine micro-albumin of the model group were significantly increased and the MDA content were increased. Therefore, the renal tissue pathological damage aggravated, and the expression of Nrf2 and HO-1, as well as its downstream target genes were all down- regulated. (P < 0.01 or P < 0.05). S. chinensis extract reduced blood glucose, 24 h urine micro-albumin and MDA level in diabetic nephropathy mice, improved renal pathological damage, and up-regulated Nrf2 and HO-1 and its downstream target gene expression. (P < 0.01 or P < 0.05). Conclusion: S. chinensis extract has protective effect on oxidative stress injury in db/db mice, and its mechanism may be related to up-regulation of antioxidant factor Nrf2 and its downstream genes.