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[1]曹木根,游濠樂,陳樂昀,等.晚期糖基化終產(chǎn)物通過TLR4/MD2通路介導(dǎo)心肌細胞炎癥的機制研究[J].福建醫(yī)藥雜志,2024,46(07):64-68.[doi:10.20148/j.fmj.2024.07.021]
　CAO Mugen,YOU Haole,CHEN Leyun,et al.Study on mechanism of AGEs mediating inflammation of cardiomyocytes through TLR4/MD2 pathway[J].FUJIAN MEDICAL JOURNAL,2024,46(07):64-68.[doi:10.20148/j.fmj.2024.07.021]
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晚期糖基化終產(chǎn)物通過TLR4/MD2通路介導(dǎo)心肌細胞炎癥的機制研究()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
46
期數(shù):
2024年07期
頁碼:
64-68
欄目:
基礎(chǔ)研究
出版日期:
2024-11-20

文章信息/Info

Title:
Study on mechanism of AGEs mediating inflammation of cardiomyocytes through TLR4/MD2 pathway
文章編號:
1002-2600(2024)07-0064-05
作者:
曹木根; 游濠樂; 陳樂昀; 魏瀟琪; 鄭煒平
福建醫(yī)科大學(xué)省立臨床醫(yī)學(xué)院 福建省立醫(yī)院老年科,福州 3500001
Author(s):
CAO Mugen;  YOU Haole;  CHEN Leyun;  WEI Xiaoqi;  ZHENG Weiping
Department of Geriatrics, Fujian Provincial Hospital, Provincial Clinical Medical College of Fujian Medical University, Fuzhou, Fujian 350001, China
關(guān)鍵詞:
晚期糖基化代謝終末產(chǎn)物;  晚期糖基化終末產(chǎn)物受體;  Toll樣受體4;  髓樣分化受體2
Keywords:
advanced glycation end products;  advanced glycation end product receptor;  toll-like receptor 4;  myeloid differentiation receptor 2
分類號:
R541
DOI:
10.20148/j.fmj.2024.07.021
文獻標(biāo)志碼:
B
摘要:
目的 探討晚期糖基化終產(chǎn)物(AGEs)通過Toll樣受體4(TLR4)/髓樣分化蛋白2(MD2)通路介導(dǎo)心肌細胞炎癥的相關(guān)機制。方法 采用不同濃度的AGEs牛血清白蛋白(0、100、200、400、800 μg/mL)干預(yù)12、24、48、60、72 h,篩選最佳的AGEs干預(yù)H9c2細胞的濃度和干預(yù)時間。將細胞分成4個組別:對照組、AGEs組、MD2抑制劑組及AGEs+MD2抑制劑組。 采用CCK-8法檢測各組細胞活力; 檢測各組乳酸脫氫酶(LDH)含量; 采用ELISA法測定各組AGEs-MD2的濃度; 使用蛋白質(zhì)印跡法檢測各組心肌細胞中TLR4下游髓樣分化因子88(MyD88)蛋白表達水平; Real time PCR法測定心肌細胞炎性相關(guān)指標(biāo)白細胞介素-6(IL-6)、腫瘤壞死因子α(TNF-α)的mRNA表達水平。結(jié)果 與對照組相比,AGEs組的細胞存活率降低,LDH釋放量升高,AGEs-MD2在450 nm處光密度增高,MyD88蛋白相對表達量增高,IL-6、TNF-α的mRNA相對表達量增高,差異有統(tǒng)計學(xué)意義(P<0.05); 與對照組相比, MD2抑制劑組細胞存活率降低,LDH釋放量升高,差異有統(tǒng)計學(xué)意義(P<0.05)。與AGEs組相比,AGEs+MD2抑制劑組的AGEs-MD2在450 nm處光密度降低,MyD88蛋白相對表達量降低,IL-6、TNF-α的mRNA相對表達量降低,差異有統(tǒng)計學(xué)意義(P<0.05)。結(jié)論 AGEs可以通過TLR4/MD2通路激活MyD88下游的炎性因子介導(dǎo)心肌細胞炎癥,這可能是體內(nèi)AGEs長期積累引起心臟重構(gòu)的機制之一。
Abstract:
Objective To explore the mechanisms by which advanced glycation end products(AGEs)mediate inflammation of cardiomyocytes through the toll-like receptor 4(TLR4)/ myeloid differentiation factor 2(MD2)pathway.Methods Intervention for 12, 24, 48, 60, 72 h was performed using different concentrations of AGEs bovine serum albumin(0, 100, 200, 400, 800 μg/mL)to identify the optimal AGEs concentration and intervention time.Subsequently, H9c2 cells were divided into four groups: control group, AGEs group, MD-2 inhibitor group, and AGEs + MD2 inhibitor group.The cell viability of H9c2 cells in each group was assessed using the CCK-8 assay.LDH levels in the culture medium of H9c2 cells were measured using a reagent kit.The concentrations of AGEs-MD2 in cardiomyocytes were measured by ELISA.The expression levels of MyD88 protein downstream of TLR4 in cardiomyocytes were detected by Western blot.The mRNA expression levels of IL-6 and TNF-α of inflammatory markers in cardiomyocytes were determined by real time PCR.Results Compared with the control group, the AGEs group showed a decrease in cell viability, an increase in LDH release, optical density at 450 nm for AGEs-MD2, relative protein expression of MyD88, and an increase in relative mRNA expression of IL-6 and TNF-α, and all the differences were statistically significant(P<0.05).Compared with the control group, the MD-2 inhibitor group showed a decrease in cell viability and an increase in LDH release,and all the differences were statistically significant(P<0.05).Compared with the AGEs group, the AGEs+MD2 inhibitor group showed a decrease in optical density at 450 nm for AGEs-MD2, a decrease in relative protein expression of MyD88, and a decrease in relative mRNA expression of IL-6 and TNF-α, and all the differences were statistically significant(P<0.05).Conclusion AGEs can activate cardimyocyte inflammation which is mediated by the inflammatory cytokines of MyD88 through the TLR4/MD2 pathway, which may be one of the mechanisms of cardiac remodeling caused by the long-term accumulation of AGEs in the body.

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相似文獻/References:

[1]魏瀟琪,王小易,林燕清,等.晚期糖基化終末產(chǎn)物與MD2-TLR4結(jié)合介導(dǎo)心臟衰老機制的研究[J].福建醫(yī)藥雜志,2021,43(01):121.
　WEI Xiaoqi,WANG Xiaoyi,LIN Yanqing,et al.Study on the mechanism of cardiac aging mediated by the combination of AGEs and MD2-TLR4[J].FUJIAN MEDICAL JOURNAL,2021,43(07):121.

備注/Memo

備注/Memo:
基金項目:福建省自然科學(xué)基金資助項目(2021J01401); 福建省衛(wèi)生廳中青年骨干基金(2018-ZQN-10)
通信作者:鄭煒平,Email:[email protected]
更新日期/Last Update: 2024-11-20