Protective Effect and Mechanism of Mori Folium Extract on Kidney of db/db Diabetic Mice
10.13422/j.cnki.syfjx.20240425
- VernacularTitle:桑叶水提物对db/db糖尿病小鼠肾脏的保护作用及其机制
- Author:
Yan HUANG
1
;
Huilin ZHANG
2
;
Changhao HE
2
;
Yongcheng AN
2
;
Wanxin FU
1
;
Menglu WANG
2
;
Ziyi SHAN
1
;
Yuhang DU
2
;
Jiamei XIE
2
;
Zhanhong JIA
2
;
Baosheng ZHAO
3
Author Information
1. College of Life Sciences， Beijing University of Chinese Medicine， Beijing 102488， China
2. College of Chinese Materia Medica， Beijing University of Chinese Medicine， Beijing 102488， China
3. Beijing Research Institute of Chinese Medicine， Beijing University of Chinese Medicine， Beijing 100029， China
- Publication Type:Journal Article
- Keywords:
Mori Folium extract;
type 2 diabetic mellitus;
diabetic nephropathy;
Toll-like receptor 4 （TLR4）;
myeloid differentiation factor 88 （MyD88）;
nuclear factor-kappa B p65 （NF-κB p65）
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2024;30(11):51-59
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the protective effects of Mori Folium extract （MLE） on the kidney of db/db diabetic mice and its mechanism. MethodTwenty-four male C57BLKS/JGpt-Leprdb/Leprdb （db/db） mice were randomly divided into model group， metformin group， low-dose group of MLE （MLE-L）， and high-dose group of MLE （MLE-H） according to their fasting blood glucose （FBG）， with six mice in each group， and other six C57BLKS/JGpt wild littermate （m/m） mice were selected as normal group. The mice in the drug administration groups were given corresponding drugs by gavage， and the mice in the normal group and model group were given the same dose of deionized water by gavage once a day for continuous eight weeks. Body weight， bilateral kidney weight， and FBG were measured， and an oral glucose tolerance test （OGTT） was performed. The pathological changes in the kidney tissue of mice were observed by hematoxylin-eosin （HE） and periodic acid-silver （PAS） staining， and serum creatinine （SCr） and blood urea nitrogen （BUN） levels were detected. Enzyme-linked immunosorbent assay （ELISA） was used to detect the levels of tumor necrosis factor-alpha （TNF-α） and interleukin-6 （IL-6） in serum and urinary microalbumin （U-mAlb） of mice. The expression levels of toll-like receptor 4 （TLR4）， myeloid differentiation factor 88 （MyD88）， and nuclear factor-kappa B p65 （NF-κB p65） protein in kidney tissue of mice were tested by Western blot. ResultCompared with the normal group， the body weight， absolute renal weight， FBG， and the area under the curve （AUC） of OGTT of mice in the model group were significantly increased （P<0.01）， and the levels of SCr， BUN， and U-mAlb， as well as TNF-α and IL-6 in serum were significantly increased （P<0.01）. The glomerular basement membrane in the kidney tissue of mice was thicker， with obvious inflammatory cell infiltration. The protein expression levels of TLR4， MyD88， and NF-κB p65 in the kidney tissue of mice were increased significantly （P<0.01）. Compared with the model group， there was no statistical difference in the body weight of mice in each drug administration group. The absolute renal weight of mice in the MLE-H and metformin groups was significantly reduced （P<0.05， P<0.01）. The FBG levels of mice in the metformin， MLE-L， and MLE-H groups started to decrease after treatment for four to eight weeks （P<0.05， P<0.01）. The AUC of mice in the MLE-H and metformin groups was significantly decreased （P<0.01）. The levels of SCr， BUN， and U-mAlb of mice in the MLE-H and metformin groups were significantly decreased （P<0.01）， and those of SCr and U-mAlb of mice in the MLE-L group were significantly decreased （P<0.01）. The levels of TNF-α and IL-6 in the serum of mice in the MLE-H and metformin groups were significantly decreased （P<0.01）. The renal tissue pathology of mice in each drug administration group was improved to varying degrees， and the protein expression levels of TLR4， MyD88， and NF-κB p65 in the MLE-H group were decreased significantly （P<0.05， P<0.01）. ConclusionMLE can improve the renal structure and function of db/db diabetic mice， and its mechanism may be related to the inhibition of the TLR4/MyD88/NF-κB signaling pathway.
