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梓醇通过抑制KDM7A促进高糖诱导的成骨细胞增殖和分化。

Catalpol Promotes the Proliferation and Differentiation of Osteoblasts Induced by High Glucose by Inhibiting KDM7A.

作者信息

Cheng Jian, Xu Hai-Yan, Liu Ming-Ming, Cai Jian-Ping, Wang Lei, Hua Zhen, Wu Xiao-Dong, Huo Wei-Ling, Lv Nan-Ning

机构信息

Department of Orthopedics, Xuzhou Central Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou, Jiangsu 221009, People's Republic of China.

Institute of Traumatology & Orthopedics, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2020 Mar 13;13:705-712. doi: 10.2147/DMSO.S246433. eCollection 2020.

DOI:10.2147/DMSO.S246433
PMID:32214833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7081648/
Abstract

INTRODUCTION

The protective effect of catalpol on diabetic osteoporosis (DOP) and its mechanism remain unclear. This study aimed to explore whether catalpol enhanced the proliferation and differentiation of MC3T3 cells induced by high glucose by inhibiting the expression of KDM7A.

METHODS

MC3T3 cells were induced by high glucose (HG) and treated with different concentrations of catalpol. The proliferation and mineralization abilities of MC3T3-E1 cells were determined by CCK-8 assay and Alizarin Red Staining, respectively. The expression of differentiation-related osteogenic proteins, KDM7A and related proteins of Wnt/β-catenin signaling pathway was analyzed by Western blot analysis. The alkaline phosphatase (ALP) activity was detected by ALP assay kits.

RESULTS

MC3T3-E1 cells induced by high glucose showed decreased proliferation and mineralization abilities and decreased ALP activity, which were all reversed by the treatment of catalpol. High glucose induction inhibited the expression of KDM7A, Total-β-catenin, Nuclear-β-catenin and p-GSK3β, which was reversed by the treatment of catalpol. And KDM7A interference up-regulated the expression of Total-β-catenin, Nuclear-β-catenin and p-GSK3β, which was down-regulated by KDM7A overexpression. Furthermore, the proliferation and mineralization abilities and ALP activity were improved when treated with KDM7A interference and decreased when treated with KDM7A overexpression. However, SKL2001 could improve the proliferation and mineralization abilities and ALP activity of MC3T3-E1 cells.

DISCUSSION

Catalpol promotes the proliferation and differentiation of osteoblasts induced by high glucose by regulating the Wnt/β-catenin signaling pathway through KDM7A.

摘要

引言

梓醇对糖尿病性骨质疏松症（DOP）的保护作用及其机制尚不清楚。本研究旨在探讨梓醇是否通过抑制KDM7A的表达来增强高糖诱导的MC3T3细胞的增殖和分化。

方法

用高糖（HG）诱导MC3T3细胞，并用不同浓度的梓醇处理。分别通过CCK-8法和茜素红染色检测MC3T3-E1细胞的增殖和矿化能力。通过蛋白质免疫印迹分析检测分化相关成骨蛋白、KDM7A以及Wnt/β-连环蛋白信号通路相关蛋白的表达。用碱性磷酸酶（ALP）检测试剂盒检测ALP活性。

结果

高糖诱导的MC3T3-E1细胞增殖和矿化能力降低，ALP活性下降，而梓醇处理可使其逆转。高糖诱导抑制了KDM7A、总β-连环蛋白、核β-连环蛋白和p-GSK3β的表达，梓醇处理可使其逆转。KDM7A干扰上调了总β-连环蛋白、核β-连环蛋白和p-GSK3β的表达，而KDM7A过表达则使其下调。此外，KDM7A干扰处理可提高细胞的增殖和矿化能力以及ALP活性，KDM7A过表达处理则使其降低。然而，SKL2001可提高MC3T3-E1细胞的增殖和矿化能力以及ALP活性。

讨论

梓醇通过KDM7A调节Wnt/β-连环蛋白信号通路，促进高糖诱导的成骨细胞增殖和分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/d58dbfa75eb8/DMSO-13-705-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/de8fa948b1bb/DMSO-13-705-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/114079205701/DMSO-13-705-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/19ede0acb61c/DMSO-13-705-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/d1471f9e8f5a/DMSO-13-705-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/d58dbfa75eb8/DMSO-13-705-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/de8fa948b1bb/DMSO-13-705-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/114079205701/DMSO-13-705-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/19ede0acb61c/DMSO-13-705-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/d1471f9e8f5a/DMSO-13-705-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6073/7081648/d58dbfa75eb8/DMSO-13-705-g0005.jpg

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