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[1]劉合亮,林煜,鄭世雄,等.青娥丸調(diào)控PERK/eIF2α/ATF4/CHOP通路對(duì)成骨細(xì)胞凋亡的影響[J].福建醫(yī)藥雜志,2025,47(03):66-71.[doi:10.20148/j.fmj.2025.03.017]
 LIU Heliang,LIN Yu,ZHENG Shixiong,et al.Mechanism of Qing'E formula regulating PERK/eIF2α/ATF4/CHOP pathway and its impact on osteoblast apoptosis[J].FUJIAN MEDICAL JOURNAL,2025,47(03):66-71.[doi:10.20148/j.fmj.2025.03.017]
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青娥丸調(diào)控PERK/eIF2α/ATF4/CHOP通路對(duì)成骨細(xì)胞凋亡的影響()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
47
期數(shù):
2025年03期
頁碼:
66-71
欄目:
基礎(chǔ)研究
出版日期:
2025-03-20

文章信息/Info

Title:
Mechanism of Qing'E formula regulating PERK/eIF2α/ATF4/CHOP pathway and its impact on osteoblast apoptosis
文章編號(hào):
1002-2600(2025)03-0066-06
作者:
劉合亮林煜鄭世雄肖莉莉
福建省福州市第二總醫(yī)院,福州 350007
Author(s):
LIU Heliang LIN Yu ZHENG Shixiong XIAO Lili
Department of Orthopedics, Fuzhou Second General Hospital, Fuzhou, Fujian 350007, China
關(guān)鍵詞:
絕經(jīng)后骨質(zhì)疏松癥 青娥丸 內(nèi)質(zhì)網(wǎng)應(yīng)激 PERK/eIF2α/ATF4/CHOP信號(hào)通路
Keywords:
postmenopausal osteoporosis Qing'E formula endoplasmic reticulum stress PERK/eIF2α/ATF4/CHOPsignaling pathway
分類號(hào):
R816.8
DOI:
10.20148/j.fmj.2025.03.017
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 基于PERK/eIF2α/ATF4/CHOP信號(hào)通路探討青娥丸含藥血清對(duì)氧化應(yīng)激誘導(dǎo)內(nèi)質(zhì)網(wǎng)應(yīng)激凋亡成骨細(xì)胞系的保護(hù)作用及其作用機(jī)制。方法 30只雄性SD大鼠隨機(jī)分為生理鹽水組和青娥丸組,每組15只,分別給予生理鹽水和青娥丸灌胃干預(yù),連續(xù)7 d,腹主動(dòng)脈取全血制備含藥血清; 培養(yǎng)UMR-106細(xì)胞株,CCK-8篩選青娥丸和GSK2606414最佳干預(yù)濃度,細(xì)胞分為空白組、模型組、青娥丸組和抑制劑組,進(jìn)一步采用10 μmol/L的H2O2干預(yù)細(xì)胞12 h制備內(nèi)質(zhì)網(wǎng)應(yīng)激模型,CCK-8檢測4組細(xì)胞的增殖活性,DCFH-DA檢測細(xì)胞活性氧(ROS)含量,Real-time PCR和Western blot檢測PERK、eIF2α、ATF4、CHOP mRNA和蛋白的相對(duì)表達(dá)量。結(jié)果 青娥丸含藥血清最佳干預(yù)濃度為10%,GSK2606414最佳干預(yù)濃度為4%,此最佳干預(yù)濃度用于后續(xù)實(shí)驗(yàn)。H2O2干預(yù)后模型組細(xì)胞增殖活性顯著降低,ROS含量顯著升高,PERK、eIF2α、ATF4、CHOP mRNA和蛋白的相對(duì)表達(dá)量顯著上調(diào); 青娥丸組增殖活性增強(qiáng),ROS含量顯著降低,PERK、eIF2α、ATF4、CHOP mRNA和蛋白的相對(duì)表達(dá)量下調(diào)。結(jié)論 青娥丸含藥血清可有效抑制成骨細(xì)胞系的內(nèi)質(zhì)網(wǎng)應(yīng)激凋亡,其作用機(jī)制可能與PERK/eIF2α/ATF4/CHOP信號(hào)通路相關(guān)。
Abstract:
Objective To examine the protective effects and its mechanism of Qing'E formula serum on osteoblast apoptosis caused by oxidative stress-induced endoplasmic reticulum stress, focusing on the PERK/eIF2α/ATF4/CHOP signaling pathway. Methods Thirty male SD rats were randomly assigned to receive either normal saline or Qing'E formula via gavage for seven days to prepare drug-containing serum from abdominal aorta blood. UMR-106 cells were cultured, CCK-8 was selected for the optimal intervention concentration of Qing'E formula and GSK2606414. Cells were categorized into blank, model, Qing'E formula, and positive drug groups. The endoplasmic reticulum stress model was created by treating cells with 10 μmol/L H2O2 for 12 hours. Cell proliferation was assessed using CCK-8, ROS levels were dectected with DCFH-DA, and the expression levels of PERK, eIF2α, ATF4, and CHOP mRNA and protein were detected through Real-time PCR and Western blot. Results The optimal concentrations for Qing'E formula serum and GSK2606414 were found to be 10% and 4%, respectively. This optimal intervention concentration was used for subsequent experiments. Post-H2O2 treatment, the model group showed reduced cell proliferation, increased ROS, and elevated PERK, eIF2α, ATF4, and CHOP expression. Conversely, the Qing'E formula group exhibited increased proliferation, reduced ROS, and decreased expression of the above related markers. Conclusion Qing'E formula serum effectively inhibits endoplasmic reticulum stress-induced apoptosis in osteoblasts, possibly through the PERK/eIF2α/ATF4/CHOP signaling pathway.

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[1]林建立,林移婷,陳耀琦,等.絕經(jīng)后骨質(zhì)疏松患者骨代謝與脂代謝的關(guān)系及血清蛋白組學(xué)研究[J].福建醫(yī)藥雜志,2025,47(02):1.[doi:10.20148/j.fmj.2025.02.001]
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備注/Memo

備注/Memo:
基金項(xiàng)目:福州市衛(wèi)健系統(tǒng)科技計(jì)劃項(xiàng)目(2021-S-wq20); 福建省科學(xué)自然基金項(xiàng)目(2022J011318); 福建省衛(wèi)生健康中青年骨干人才培養(yǎng)項(xiàng)目(2020GGB046); 福建省科技創(chuàng)新平臺(tái)項(xiàng)目(福建省創(chuàng)傷骨科急救與康復(fù)臨床醫(yī)學(xué)研究中心,2020Y2014)
通信作者:鄭世雄,Email:[email protected]
更新日期/Last Update: 2025-03-20