柿叶黄酮对糖尿病肾病大鼠血糖值及肾组织中TGF-和MMP-9的影响

零伟德; 杜刚

doi:10.13422/j.cnki.syfjx.2016160139

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柿叶黄酮对糖尿病肾病大鼠血糖值及肾组织中TGF-和MMP-9的影响

药理 | 更新时间：2024-01-04

- 柿叶黄酮对糖尿病肾病大鼠血糖值及肾组织中TGF-和MMP-9的影响
- Effect of Flavonoid from Leaves on TGF- and MMP-9 in Blood Glucose Levels and Kidney Tissues of Rats with Diabetic Nephropathy
- 中国实验方剂学杂志 2016年22卷第16期页码：139-143
- 作者机构：
- 作者简介：
- 基金信息：
  
  广西自然科学基金青年项目（2013JJBA40062）
- DOI：10.13422/j.cnki.syfjx.2016160139
  中图分类号： R285.5
- 纸质出版日期：2016
- 稿件说明：
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零伟德, 杜刚. 柿叶黄酮对糖尿病肾病大鼠血糖值及肾组织中TGF-和MMP-9的影响[J]. 中国实验方剂学杂志, 2016,22(16):139-143.

LING Wei-de, DU Gang. Effect of Flavonoid from Leaves on TGF- and MMP-9 in Blood Glucose Levels and Kidney Tissues of Rats with Diabetic Nephropathy[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(16): 139-143.
零伟德, 杜刚. 柿叶黄酮对糖尿病肾病大鼠血糖值及肾组织中TGF-和MMP-9的影响[J]. 中国实验方剂学杂志, 2016,22(16):139-143. DOI： 10.13422/j.cnki.syfjx.2016160139.

LING Wei-de, DU Gang. Effect of Flavonoid from Leaves on TGF- and MMP-9 in Blood Glucose Levels and Kidney Tissues of Rats with Diabetic Nephropathy[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(16): 139-143. DOI： 10.13422/j.cnki.syfjx.2016160139.

摘要

目的：观察柿叶黄酮对大鼠糖尿病肾组织中转化生长因子-β1（TGF-β1）和基质金属蛋白酶-9（MMP-9）的影响，并探讨其作用机制。方法： 50只SD大鼠ip链脲佐菌素（STZ）溶液120 mg·kg-1，对大鼠进行糖尿病大鼠模型造模。随机将造模成功大鼠分为模型组，氨基胍组（0.1 g·kg-1·d-1），柿叶黄酮高、中、低剂量组（400，200，100 mg·kg-1），每组10只大鼠，另设正常组大鼠10只。氨基胍组、柿叶黄酮组ig给药（1次/天），连续给药12周，期间给予模型组和正常组等体积生理盐水。给药前及给药期间每隔3周测大鼠24 h尿蛋白含量及空腹血糖（FBG），末次给药2 h后处死大鼠，苏木素-伊红（HE）染色观察肾脏病理学变化，采用生化仪测定肾组织匀浆中丙二醛（MDA），超氧化物歧化酶（SOD），糖基化终产物（AGEs）及果糖胺（FTS）水平，蛋白质免疫印迹（Western blot）法检测肾脏组织中TGF-β1和MMP-9的蛋白表达。结果：与正常组比较，模型组中大鼠24 h尿蛋白含量及FBG含量持续增高，肾组织中MDA，AGEs，FTS含量升高明显，SOD水平明显下降（P<0.05，P<0.01）；与模型组比较，柿叶黄酮各剂量组明显降低24 h尿蛋白含量及FBG含量及肾组织中MDA，AGEs，FTS含量，明显升高SOD水平（P<0.05，P<0.01），明显下调肾脏组织中TGF-β1和上调MMP-9的蛋白水平（P<0.05），其中柿叶黄酮高剂量组作用较为明显。结论：柿叶黄酮对糖尿病肾病大鼠有一定保护作用，其机制与柿叶黄酮的降糖、降脂、降低氧化应激水平及非酶糖基化的作用以及抑制TGF-β1和MMP-9蛋白相关。

Abstract

Objective: To investigate the protective mechanism of flavonoid from Diospyros kaki leaves (FDKL) on transforming growth factor-β1(TGF-β1) and matrix metalloproteinase-9(MMP-9) of diabetic nephropathy(DN) rats. Method: The 50 DN rats were intraperitoneally injected with streptozotocin(STZ) (120 mg·kg-1) to establish the rat diabetic model. The blood glucose was measured before modeling

and the DN rats were randomly divided into model group

aminoguanidine group

FDKL low

medium and high-dose (100

200

400 mg·kg-1) groups

with 10 rats in each group. Normal group was composed of 10 normal rats. The rats were administrated with the corresponding medicines for 12 weeks

and the rats of normal and model groups were given equal volume of normal saline. Before and during the administration

the 24 h urine protein and fasting blood glucose (FBG) were determined every 3 weeks. Two hours later after the last administration

the levels of methane dicarboxylic aldehyde (MDA)

superoxide dismutase (SOD)

advanced glycation end products (AGEs) and fructosamine (FTS) in kidney tissues were tested after the treatment. The changes of kidney morphology were tested through HE-staining. The expressions of TGF-β1 and MMP-9 in kidney tissues were detected using Western blot. Result: Compared with the normal group

the model group showed continuous increase in 24 h urine protein and FBG content

and the levels MDA

AGEs

FTS in kidney tissues

and significantly decrease in SOD (P<0.05

P<0.01).Compared with the model group

all of FDKL groups showed significant reduction in 24 h urine protein and the levels MDA

AGEs

FTS in kidney tissues

and significant increase in SOD (P<0.05

P<0.01)

notable decrease in TGF-β1 in kidney tissues

and up-regulation in MMP-9 (P<0.05)

particularly FDKL high-dose group. Conclusion: FDKL has a protective effect on diabetic nephropathy rats

and its mechanisms are associated with the decrease in blood glucose

lipid

oxidative stress and non-enzymatic glycosylation and the inhibition of TGF-β1 and MMP-9 proteins.

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