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高良姜素对膝关节炎大鼠软骨细胞自噬和凋亡的影响
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| 篇名： | 高良姜素对膝关节炎大鼠软骨细胞自噬和凋亡的影响 |
| TITLE： | Effects of galangin on autophagy and apoptosis of chondrocytes in knee osteoarthritis rats |
| 摘要： | 目的 探讨高良姜素（GLA）调节腺苷一磷酸活化的蛋白质激酶（AMPK）/哺乳动物雷帕霉素靶蛋白（mTOR）/UNC-51样激酶1（ULK1）信号通路对膝关节炎（KOA）大鼠软骨细胞自噬和凋亡的影响。方法构建KOA大鼠模型，将其分为模型组，GLA低、中、高剂量组（皮下注射100、200、400μg/kg的GLA），GLA+CompoundC组（皮下注射400μg/kg的GLA+0.2mg/kg的AMPK抑制剂CompoundC），每组10只；另选取10只正常饲养的大鼠作为假手术组。末次给药后，检测大鼠膝关节肿胀程度，观察大鼠膝关节软骨组织病理学；检测大鼠血清中基质金属蛋白酶13（MMP-13）、白细胞介素1β（IL-1β）水平；观察大鼠骨细胞自噬情况；检测大鼠软骨细胞凋亡情况；检测大鼠膝关节软骨组织中AMPK/mTOR/ULK1信号通路相关蛋白磷酸化水平。结果与假手术组相比，模型组大鼠关节软骨细胞排列紊乱，细胞核固缩，关节软骨层纤维化严重，且伴有大量炎症细胞浸润；膝关节肿胀程度，软骨细胞自噬空泡数、凋亡率，血清中MMP-13、IL-1β水平，膝关节软骨组织中mTOR蛋白的磷酸化水平均显著升高（P＜0.05）；膝关节软骨组织中AMPK、ULK1蛋白的磷酸化水平均显著降低（P＜0.05）。与模型组相比，GLA低、中、高剂量组大鼠膝关节软骨损伤明显改善，炎症细胞浸润减轻，上述定量指标除自噬空泡数进一步升高外均显著逆转，且具有剂量依赖性（P＜0.05）。与GLA高剂量组比较，GLA+CompoundC组大鼠膝关节软骨损伤和炎症细胞浸润加重，上述定量指标均显著逆转（P＜0.05）。结论GLA可促进KOA大鼠软骨细胞自噬，抑制细胞凋亡，其作用机制可能与激活AMPK/mTOR/ULK1信号通路有关。 |
| ABSTRACT： | OBJECTIVE To investigate the effects of galangin （GLA） on autophagy and apoptosis of chondrocytes in knee osteoarthritis （KOA） rats by regulating the adenosine monophosphate-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR）/UNC-51-like kinase 1 （ULK1） signaling pathway. METHODS KOA rat model was constructed and separated into model group， L-GLA， M-GLA， H-GLA groups [subcutaneous injection of 100， 200， 400 μg/kg GLA]， GLA+Compound C group [subcutaneous injection of 400 μg/kg GLA+0.2 mg/kg AMPK inhibitor Compound C]， with 10 rats in each group. Additionally， 10 normally fed rats were selected as the sham operation group. After the last medication， the degree of knee joint swelling of rats in each group was detected； the pathology of knee joints in KOA rats was observed. The serum expressions of matrix metalloproteinase 13 （MMP-13） and interleukin-1β （IL-1β） in KOA rats were detected； the autophagy of chondrocytes in KOA rats was observed； the chondrocyte apoptosis in KOA rats was detected； the phosphorylation of AMPK/mTOR/ULK1 pathway-related proteins in cartilage tissue of knee joint were detected in rats. RESULTS Compared with the sham operation group， the arrangement of articular chondrocytes in the model group was disordered， with nuclear pyknosis and severe fibrosis of the articular cartilage layer， accompanied by a large amount of inflammatory cell infiltration； the degree of joint swelling， the number of autophagic vacuoles and apoptosis rate of chondrocytes， serum levels of MMP-13 and IL-1β， and the phosphorylation of mTOR protein in cartilage tissue of knee joint were all increased significantly （P＜0.05）， while the phosphorylation of AMPK and ULK1 protein were all decreased significantly in cartilage tissue of knee joint （P＜0.05）. Compared with the model group， L- GLA， M-GLA， H-GLA groups showed significant improvement in joint cartilage injury and reduced infiltration of inflammatory cells in rats. The above quantitative indicators were significantly reversed in a dose-dependent manner，except the number of autophagic vacuoles increased significantly （P＜0.05）. Compared with the H-GLA group， the GLA+ Compound C group showed aggravated cartilage tissue of joint cartilage injury and inflammatory cell infiltration in rats， and the above quantitative indicators were reversed significantly （P＜0.05）. CONCLUSIONS GLA can promote autophagy and inhibit apoptosis of chondrocytes in KOA rats， the mechanism of which may be associated with activating AMPK/mTOR/ULK1 signaling pathway. |
| 期刊： | 2025年第36卷第03期 |
| 作者： | 杨青；黄伟；刘清毅；周仲瑜 |
| AUTHORS： | YANG Qing，HUANG Wei，LIU Qingyi，ZHOU Zhongyu |
| 关键字： | 高良姜素；膝关节炎；软骨细胞；自噬；凋亡；AMPK/mTOR/ULK1信号通路 |
| KEYWORDS： | galangin； knee osteoarthritis； chondrocytes； autophagy； apoptosis； AMPK/mTOR/ULK1 signaling pathway |
| 阅读数： | 4 次 |
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