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京尼平苷通过PI3K/Akt通路促进糖尿病大鼠皮肤溃疡创面愈合

姜雯雯 刘欢 陈晓燕 荣小娟 刘燕玲 曾威

中国比较医学杂志2023,Vol.33Issue(12):14-20,7.
中国比较医学杂志2023,Vol.33Issue(12):14-20,7.DOI:10.3969/j.issn.1671-7856.2023.12.003

京尼平苷通过PI3K/Akt通路促进糖尿病大鼠皮肤溃疡创面愈合

Geniposide promotes skin ulcer wound healing in diabetic rats through the PI3K/Akt pathway

姜雯雯 1刘欢 1陈晓燕 1荣小娟 1刘燕玲 1曾威1

作者信息

  • 1. 江西科技学院医学院,南昌 330098
  • 折叠

摘要

Abstract

Objective To investigate the protective effect of geniposide against diabetic rats with skin ulcer and the mechanism.Methods Rats were divided into a normal group,model group,and geniposide subgroups(Gen(L):200 mg/kg;Gen(H):500 mg/kg).Diabetic rats were treated with normal saline or geniposide by intragastric administration(n=6).Treatments were administered once a day,and the wound healing and inflammation of each group were recorded every day.After 7 days of treatment for diabetic skin ulcers,the wound area,tissue sections,TUNEL staining and Western blot were used to quantitatively analyze changes in wound healing,apoptosis,and related regulatory protein expression.Results Compared with the model group,the group receiving orally administered geniposide(200 and 500 mg/kg)showed significantly improved wound healing and increased contraction of the injured area.In terms of skin wound apoptosis in diabetic rats,TUNEL-positive cells were significantly reduced in geniposide subgroups(P<0.05).Geniposide significantly inhibited skin inflammation and promoted wound repair,which may be related to promotion of PI3K and Akt phosphorylation.Conclusions Geniposide promoted skin wound repair in diabetic rats by inhibiting inflammatory responses and apoptosis.

关键词

京尼平苷/糖尿病性皮肤溃疡/PI3K/Akt/细胞凋亡

Key words

geniposide/diabetic skin ulcer/PI3K/Akt/cell apoptosis

分类

医药卫生

引用本文复制引用

姜雯雯,刘欢,陈晓燕,荣小娟,刘燕玲,曾威..京尼平苷通过PI3K/Akt通路促进糖尿病大鼠皮肤溃疡创面愈合[J].中国比较医学杂志,2023,33(12):14-20,7.

基金项目

江西省中医药管理局科技计划项目(2023A0367) (2023A0367)

江西省卫生健康委科技计划项目(202311153) (202311153)

江西科技学院校级自然科学项目(23ZRZD05) (23ZRZD05)

江西省教育厅科学技术研究项目(GJJ202016). (GJJ202016)

中国比较医学杂志

OA北大核心CSTPCD

1671-7856

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