-
Seabuckthorn polysaccharide alleviates insulin resistance, liver and kidney function damage in diabetic rats by inhibiting PERK/ATF4/CHOP pathway
- Yao Lan, Jiang Chengxia, Guo Yanyan, You Chengshan, Li Mei, Ye Xujuan
-
Chinese Journal of Clinical Anatomy. 2021, 39(2):
187-191.
doi:10.13418/j.issn.1001-165x.2021.02.013187
-
Abstract
(
641 )
PDF (5343KB)
(
38
)
-
References |
Related Articles |
Metrics
Objective To investigate the effects of seabuckthorn polysaccharide (SP) on insulin resistance, liver and kidney function damage in diabetic rats. Methods Rats were randomly divided into the following groups: a control group, a streptozocin (STZ) group, a rosiglitazone (RSG) group (4 mg.kg-1.d-1) and a low, a medium and a high dose SP group (50, 100, 200 mg.kg-1.d-1). All rats except the control group were established as type II diabetes model. After drug treatment, the body weight, bilateral kidney weight, fasting blood sugar and insulin levels were measured by balance, blood glucose meter and Elisa, and renal hypertrophy index and insulin resistance index were calculated. The levels of HbA1C and adiponectin were detected by Elisa, and the levels of TG, TC, LDL-C, HDL-C, PRO, Scr and BUN were detected by biochemical analyzer. Oil red O and HE staining were used to observe hepatic fat deposition and renal histomorphology. Western Blot was used to detect the activation level of PERK/ATF4/CHOP pathway. Results Compared with the model group, the body weight, adiponectin and HDL-C content in the medium and high doses of SP group significantly increased (P<0.05). While the blood glucose content, insulin resistance index, kidney hypertrophy index, HbA1C, plasma insulin, the levels of TG, TC, LDL-C, proteinuria, Scr, BUN in the medium and high doses of SP group significantly down-regulated (P<0.05). SP could alleviate liver lipid deposition and kidney damage, and inhibit the activity of PERK/ATF4/CHOP pathway in rats. Conclusions Seabucthorn Polysaccharide can alleviate insulin resistance, liver and kidney function damage in diabetic rats, its mechanism may be related to the inhibition of PERK/ATF4/CHOP pathway activity.