Mechanism of Hedysari Radix Polysaccharide on Diabetic Nephropathy in db/db Mice Based on JAK2/STAT3 Signaling Pathway
10.13422/j.cnki.syfjx.20230106
- VernacularTitle:基于JAK2/STAT3信号通路探讨红芪多糖对糖尿病肾病db/db小鼠作用机制
- Author:
Yanxu CHEN
1
;
Zhisheng JIN
1
;
Xiaoxue JIANG
1
;
Boling ZHANG
1
;
Yaoqin FU
1
;
Caiyun JIN
1
;
Qinyuan ZHANG
1
;
Changqing XU
1
Author Information
1. Gansu University of Chinese Medicine，Lanzhou 730030，China
- Publication Type:Journal Article
- Keywords:
Hedysari Radix polysaccharide;
diabetic nephropathy;
Janus kinase 2 （JAK2）;
signal transducer and activator of transcription protein 3 （STAT3）;
suppressor of cytokine signaling 3 （SOCS3）;
tumor necrosis factor-α （TNF-α）
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2023;29(13):65-71
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo observe the effect of Hedysari Radix polysaccharide （HRP） on the Janus kinase 2 （JAK2）/signal transducer and activator of transcription protein 3 （STAT3） signaling pathway in diabetic nephropathy db/db mice. MethodFifty db/db mice were randomly divided into model group， irbesartan group （irbesartan suspension， 22.75 mg·kg-1）， and high-， medium-， and low-dose HRP groups （HRP suspension， 200， 100， 50 mg·kg-1） according to the body weight， with 10 mice in each group. Another 10 C57BL/6 mice were assigned to the normal group. The mice were treated with corresponding drugs by gavage， while those in the normal group and the model group received distilled water at 5 mL·kg-1. The mice in the six groups were administered once a day by gavage for 12 consecutive weeks. The uric acid （UA）， triglycerides （TG）， and total cholesterol （TC） were detected. Periodic acid-Schiff （PAS） staining and Masson staining were used to observe the pathological changes in kidney tissues. Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect the protein and mRNA expression levels of JAK2， STAT3， suppressor of cytokine signaling 3 （SOCS3）， and tumor necrosis factor-α （TNF-α） in the kidney. ResultAfter 12 weeks of treatment， compared with the normal group， the model group showed significant pathological ultrastructural changes in kidney tissues and increased UA， TG， and TC levels （P<0.01）. Compared with the model group， the high- and medium-dose HRP groups and the irbesartan group showed improvement in pathological ultrastructure of kidney tissues and reduced UA， TG， and TC levels （P<0.05， P<0.01）. Compared with the normal group， the model group showed a decrease in SOCS3 protein and mRNA expression levels and an increase in JAK2， STAT3， and TNF-α protein and mRNA expression levels （P<0.01）. Compared with the model group， the high- and medium-dose HRP groups and the irbesartan group showed an increase in SOCS3 protein and mRNA expression levels and a decrease in JAK2， STAT3， and TNF-α protein and mRNA expression levels （P<0.05， P<0.01）. ConclusionHRP can alleviate renal damage in diabetic nephropathy to a certain extent， and its mechanism may be related to the inhibition of the activation of the JAK2/STAT3 signaling pathway.
