Effects of polysaccharides from Endothelium Corneum Gigeriae Galli on high glucose⁃induced islet β cell activity and Nrf2 signaling pathway

DING Yerong; ZHOU Chunnan; WANG Yuanming

doi:10.16305/j.1007-1334.2024.z20240602001

您当前的位置：

首页 >

文章列表页 >

Effects of polysaccharides from Endothelium Corneum Gigeriae Galli on high glucose⁃induced islet β cell activity and Nrf2 signaling pathway

更新时间：2024-11-07

- Effects of polysaccharides from Endothelium Corneum Gigeriae Galli on high glucose⁃induced islet β cell activity and Nrf2 signaling pathway
- Shanghai Journal of Traditional Chinese Medicine Vol. 58, Issue 11, Pages: 90-96(2024)
- 作者机构：
  
  1.兰州市七里河区人民医院公卫科（甘肃兰州 730050）
  2.甘肃中医药大学附属医院内分泌科（甘肃兰州 730200）
- 作者简介：
- 基金信息：
- DOI：10.16305/j.1007-1334.2024.z20240602001
  CLC：
- Published：10 November 2024，
  
  Received：02 June 2024，
- 稿件说明：
移动端阅览
丁叶蓉,周春楠,王苑铭.鸡内金多糖对高糖诱导的胰岛β细胞活性和Nrf2信号通路的影响[J].上海中医药杂志,2024,58(11):90-96.

DING Yerong,ZHOU Chunnan,WANG Yuanming.Effects of polysaccharides from Endothelium Corneum Gigeriae Galli on high glucose⁃induced islet β cell activity and Nrf2 signaling pathway[J].Shanghai Journal of Traditional Chinese Medicine,2024,58(11):90-96.
丁叶蓉,周春楠,王苑铭.鸡内金多糖对高糖诱导的胰岛β细胞活性和Nrf2信号通路的影响[J].上海中医药杂志,2024,58(11):90-96. DOI： 10.16305/j.1007-1334.2024.z20240602001.

DING Yerong,ZHOU Chunnan,WANG Yuanming.Effects of polysaccharides from Endothelium Corneum Gigeriae Galli on high glucose⁃induced islet β cell activity and Nrf2 signaling pathway[J].Shanghai Journal of Traditional Chinese Medicine,2024,58(11):90-96. DOI： 10.16305/j.1007-1334.2024.z20240602001.

摘要

目的

探究鸡内金多糖对高糖诱导后胰岛β细胞相关活性和对超氧化物歧化酶（SOD）、丙二醛（MDA）以及核因子E2相关因子2（Nrf2）等相关指标所产生的影响。

方法

取胰岛β细胞MIN6，培养检测其活性后分为正常组（5.5 mmol·Ｌ

-1

正常糖处理4 h）、高糖组（高脂高糖处理1 h，33.3 mmol·Ｌ

-1

葡萄糖+0.25 mmol·Ｌ

-1

棕榈酸）、鸡内金多糖低剂量组（20 μmol·L

-1

鸡内金多糖预处理4 h+高脂高糖处理24 h）、鸡内金多糖高剂量组（80 μmol·L

-1

鸡内金多糖预处理4 h+高脂高糖处理24 h），采用5-乙炔基-2′脱氧尿嘧啶核苷（EdU）检测各组细胞增殖率，缺口末端标记法（TUNEL）检测细胞凋亡，分析细胞周期，细胞划痕实验检测MIN6细胞迁移功能，检测MIN6细胞培养液中SOD、MDA水平，免疫印迹法检测MIN6细胞中Nrf2、醌氧化还原酶1（NQO1）和血红素单加氧酶-1（HO-1）蛋白表达，实时荧光定量逆转录聚合酶链式反应（RT-qPCR）检测MIN6细胞中

Nrf2

、

‑

、

NQO1

mRNA表达。

结果

与正常组比较，高糖组MIN6细胞增殖率，SOD及

Nrf2

、

NQO1

mRNA和蛋白均降低，MDA及细胞凋亡率升高（

0.05）；与高糖组比较，鸡内金多糖低剂量组MIN6细胞增殖率，SOD及

Nrf2

、

NQO1

mRNA和蛋白升高、MDA及细胞凋亡率降低（

0.05）；与鸡内金多糖低剂量组比较，鸡内金多糖高剂量组MIN6细胞增殖率，SOD及

Nrf2

、

NQO1

mRNA和蛋白升高，MDA及细胞凋亡率降低（

0.05）。与正常组比较，高糖组MIN6细胞周期G

升高，S、G

/M降低（

0.05）；与高糖组比较，鸡内金多糖低剂量组MIN6细胞周期G

降低，S和G

/M升高（

0.05）；与鸡内金多糖低剂量组比较，鸡内金多糖高剂量组MIN6细胞周期G

降低，S、G

/M升高（

0.05）。划痕结果显示，0 h各组空白区无差异；24 h高糖组空白区增大；鸡内金多糖低剂量组空白区域有所缩小；鸡内金多糖高剂量组空白区域总体显著变窄。

结论

鸡内金多糖能够促进胰岛β细胞MIN6的增殖，抑制其凋亡，可能与抑制Nrf2等相关通路相关。

Abstract

Objective

To investigate the effects of polysaccharides from Endothelium Corneum Gigeriae Galli （PECG）on the activity of islet β cells induced by high glucose， superoxide dismutase （SOD）， malondialdehyde （MDA） and nuclear factor E2 related factor 2 （Nrf2）.

Methods

Islet β cells MIN6 were cultured to detect their activity and then divided into normal group （5.5 mmol·L

-1

normal glucose treatmentfor for 4 h） and high glucose group （high lipid and high glucose treatment for 1 h， 33.3 mmol·L

-1

glucose +0.25 mmol·L

-1

palmitic acid）， low dose of PECG （20 μmol·L

-1

PECG pretreatment for 4 h+ high fat and high sugar treatment for 24 h）， high dose of PECG （80 μmol·L

-1

PECG pretreatment for 4 h+ high fat and high sugar treatment for 24 h）， cell proliferation rate was detected by 5-acetylidene-2' deoxyuracil ribonucleoside （EdU）， apoptosis was detected by notch end labeling （TUNEL）， cell cycle was analyzed， and migration function of MIN6 cells was detected by cell scratch assay. The levels of SOD and MDA in MIN6 cell culture medium were detected， and the protein expressions of Nrf2， quinone oxidoreductase 1 （NQO1） and heme monooxygenase-1 （HO-1） in MIN6 cells were detected by Western blot. Real-time fluorescence quantitative reverse transcription polymerase chain reaction （RT-qPCR） was used to detect

Nrf2

，

HO⁃1

and

NQO1

mRNA expression in MIN6 cells.

Results

Compared with the normal group， the high-glucose group showed decreased cell proliferation of MIN6 cells， as well as reduced levels of SOD and decreased expression of

Nrf2

，

， and

NQO1

mRNA and proteins. Additionally， there were increases in MDA levels and cell apoptosis （

0.05）. Relative to the high-glucose group， the low-dose PECG group showed higher proliferation of MIN6 cells and elevated levels of SOD， as well as increased expression of

Nrf2

，

， and

NQO1

mRNA and proteins. It also showed lower MDA levels and reduced cell apoptosis （

0.05）. Compared with the low-dose PECG group， the high-dose PECG group showed increased proliferation of MIN6 cells， elevated levels of SOD， and increased expression of

Nrf2

，

， and

NQO1

mRNA and proteins. There were reductions in MDA levels and cell apoptosis （

0.05）. Compared with the normal group， the high-glucose group showed an increased G

phase and decreased S and G

/M phases in the cell cycle of MIN6 cells （

0.05）. Compared with the high-glucose group， the low-dose PECG group showed a decrease in the G

phase and increases in the S and G

/M phases （

0.05）. Compared with the low-dose PECG group， the high-dose PECG group showed further reductions in the G

phase and increases in the S and G

/M phases （

0.05）. The scratch assay results revealed no differences in the gap area at 0 h among all groups. However， at 24 h， the gap area in the high-glucose group increased， whereas it decreased in the low-dose PECG group and was significantly narrowed in the high-dose PECG group.

Conclusion

PECG can promote the proliferation of MIN6 islet β cells and inhibit their apoptosis， and the effect is likely associated with the suppression of the Nrf2 signaling pathway and related pathways.

关键词

糖尿病鸡内金多糖胰岛β细胞核因子E2相关因子作用机制中药研究

Keywords

diabetes mellituspolysaccharides from Endothelium Corneum Gigeriae Galli （PECG）islet β cellnuclear factor E2-related factor （Nrf2）mechanism of actiontraditional Chinese herbal medicine research

references

ESCOTT G M， DA SILVEIRA L G， CANCELIER V D A， et al. Monitoring and management of hyperglycemia in patients with advanced diabetic kidney disease［J］. J Diabetes Complications， 2021， 35（2）： 107774.

KHUNTI S， KHUNTI K， SEIDU S. Therapeutic inertia in type 2 diabetes： prevalence， causes， consequences and methods to overcome inertia［J］. Ther Adv Endocrinol Metab， 2019，10： 2042018819844694.

黄慧，许嘉慧，陆灏. 中医药通过改善“时钟重置”防治2型糖尿病的研究进展［J］. 上海中医药杂志， 2024， 58（4）： 92-95.

国家药典委员会. 中华人民共和国药典（2020年版）：一部［M］. 北京：中国医药科技出版社， 2020： 202， 495-496．

王宝庆，郭宇莲，练有扬，等. 鸡内金化学成分及药理作用研究进展［J］. 安徽农业科学， 2017， 45（33）： 137-139.

LI Y， DUAN J Z， HE Q， et al. miR-155 modulates high glucose⁃induced cardiac fibrosis via the Nrf2/HO-1 signaling pathway［J］. Mol Med Rep， 2020， 22（5）： 4003-4016.

ZHI S M， FANG G X， XIE X M， et al. Melatonin reduces OGD/Rinduced neuron injury by regulating redox/inflammation/apoptosis signaling［J］. Eur Rev Med Pharmacol Sci， 2020， 24（3）： 1524-1536.

蒋长兴，蒋顶云，熊清平，等. 鸡内金多糖对糖尿病高脂血症大鼠血脂、血糖及细胞免疫功能的影响［J］.中国实验方剂学杂志， 2012， 18（20）： 255-258.

TOREN E ， BURNETTE K L S ， BANERJEE R R，et al. Partners in crime： beta-cells and autoimmune responses complicit in type 1 diabetes pathogenesis［J］.Front Immunol， 2021， 7（12）： 756548.

PAN Y， FU M， CHEN X， et al. Dietary methionine restriction attenuates renal ischaemia/reperfusion-induced myocardial injury by activating the CSE/H2S/ERS pathway in diabetic mice［J］. J Cell Mol Med， 2020， 24（17）： 9890-9897.

BOSMA K J， ANDREI S R， KATZ L S， et al. Pharmacological blockade of the EP3 prostaglandin E2 receptor in the setting of type 2 diabetes enhances β-cell proliferation and identity and relieves oxidative damage［J］. Mol Metab， 2021， 54： 101347.

BLENCOWE M ， FURTERER A ， WANG Q ， et al. IAPP-induced beta cell stress recapitulates the islet transcriptome in type 2 diabetes［J］. Diabetologia， 2022， 65（1）：173-187.

WANG C， ZHU L， YUAN W， et al. Diabetes aggravates myocardial ischaemia reperfusion injury via activating Nox2-related programmed cell death in an AMPK-dependent manner［J］. J Cell Mol Med， 2020， 24（12）： 6670-6679.

ZHANG D， HE Y， YE X， et al. Activation of autophagy inhibits nucleotide-binding oligomerization domain-like receptor protein 3 inflammasome activation and attenuates myocardial ischemia-reperfusion injury in diabetic rats［J］. J Diabetes Investig， 2020， 11（5）： 1126-1136.

LI W， LI W， LENG Y， et al. Mechanism of N-acetylcysteine in alleviating diabetic myocardial ischemia reperfusion injury by regulating PTEN/Akt pathway through promoting DJ-1［J］. Biosci Rep， 2020， 40（6）： BSR20192118.

GASSLER A， QUICLET C， KLUTH O， et al. Overexpression of Gjb4 impairs cell proliferation and insulin secretion in primary islet cells［J］. Mol Metab， 2020， 41： 101042.

RUBIO-NAVARRO A， GÓMEZ-BANOY N， STOLL L， et al. A beta cell subset with enhanced insulin secretion and glucose metabolism is reduced in type 2 diabetes［J］. Nat Cell Biol， 2023， 25（4）： 565-578.

王会，金平，梁新合，等. 鸡内金化学成分和药理作用研究［J］. 吉林中医药， 2018， 38（9）： 1071-1073.

KANG E， LEE J， SEO S， et al. Regulation of anti-inflammatory and antioxidant responses by methanol extract of Mikania cordata （Burm. f.） B. L. Rob. leaves via the inactivation of NF-κB and MAPK signaling pathways and activation of Nrf2 in LPS-induced RAW 264.7 macrophages［J］. Biomed Pharmacother， 2023， 168（1）：115746.

POUSO-VÁZQUEZ E， BAI X， BATALLÉ G， et al. Effects of heme oxygenase 1 in the molecular changes and neuropathy associated with type 2 diabetes in mice［J］. Biochem Pharmacol， 2022， 199（1）： 114987.

Views

下载量

CSCD

CNKI被引量

Alert me when the article has been cited

提交

Tools

Publicity Resources

Research progress on mechanisms of Huangqi⁃Huanglian herb pair and its active components in treating diabetic nephropathy

Mechanism and research progress of Atractylodis Rhizoma tonifying spleen and resolving dampness

Ancient and modern application and key information research of classic famous formula Xiangsu Powder

Ancient and contemporary textual and key informations analysis and examination of classic famous formula Shaoyao Tang

Related Author

QIN Lina

YU Rong

CHEN Qingguang

HOU Ruifang

TAO Lewei

XU Peiying

LU Hao

JIN Xin

Related Institution

Department of Endocrinology， The First Affiliated Hospital of Hunan University of Chinese Medicine

Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine

Pharmacy Department,Second Affiliated Hospital of Hunan University of Traditional Chinese Medicine

Department of Gynaecology,Second Affiliated Hospital of Hunan University of Traditional Chinese Medicine

Traditional Chinese Medicine College， Henan University of Chinese Medicine

⁰