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调中化湿汤通过p62信号通路恢复内质网自噬对胃食管反流病的改善作用机制
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| 篇名： | 调中化湿汤通过p62信号通路恢复内质网自噬对胃食管反流病的改善作用机制 |
| TITLE： | Mechanism of Tiaozhong huashi decoction in improving gastroesophageal reflux disease by restoring endoplasmic reticulum autophagy through p62 signaling pathway |
| 摘要： | 目的 探讨调中化湿汤通过p62信号通路调控大鼠食管Cajal间质细胞（ICC）内质网自噬，从而改善胃食管反流病（GERD）的分子机制。方法通过弱酸灌胃法及饮食不节法构建大鼠GERD模型后，随机分为模型组、西药组[莫沙必利1.56mg/（kg·d）、兰索拉唑3.125mg/（kg·d）]及调中化湿汤低、中、高剂量[4.713、9.425、18.85g/（kg·d）]组，另设空白组，每组8只。各组大鼠每日灌胃相应药液或生理盐水2次，连续14d。干预期间，观察大鼠毛发、精神状态、饮食量、排便等一般情况。末次干预后，观察大鼠食管组织病理变化和ICC超微结构，检测食管组织中p62、自噬相关蛋白8（ATG8）、200kDaFAK家族激酶相互作用蛋白（FIP200）、Unc-51样自噬激活激酶1（ULK1）蛋白相对表达量和阳性表达水平。结果与空白组比较，模型组大鼠精神萎靡，食管基底层增厚、固有层乳头延长并伴炎症细胞浸润，内质网显著扩张呈圆泡状囊池，伴核糖体脱落，并见少量自噬小体积聚；p62、ATG8、FIP200、ULK1蛋白相对表达量和阳性表达水平均显著降低（P＜0.05）。与模型组比较，调中化湿汤中、高剂量组大鼠上述病理损伤均有不同程度改善，受损内质网结构得以修复，未见自噬小体积聚，其中调中化湿汤中剂量组大鼠食管组织中p62、ATG8、FIP200、ULK1蛋白相对表达量和阳性表达水平均显著升高（P＜0.05）。结论调中化湿汤可改善GERD大鼠食管黏膜损伤，其作用机制可能与激活p62信号通路、修复ICC内质网结构形态及自噬能力有关。 |
| ABSTRACT： | OBJECTIVE To investigate the molecular mechanism of Tiaozhong huashi decoction in improving gastroesophageal reflux disease （GERD） by regulating endoplasmic reticulum autophagy in rat esophageal interstitial cells of Cajal （ICC） through p62 signaling pathway.METHODS After establishing a rat GERD model via the weak acid intragastric administration and irregular diet， the rats were randomly divided into model group， western medicine group [1.56 mg/（kg·d） of mosapride， 3.125 mg/（kg·d） of lansoprazole] and low-， medium- and high-dose Tiaozhong huashi decoction [4.713， 9.425， 18.85 g/（kg·d）] groups. A blank group was also set up， with 8 rats in each group. The rats in each group were intragastrically administered with corresponding liquid or normal saline twice a day for 14 days. During the intervention period， the general conditions of rats’ hair， spirit， diet and defecation were observed. After the last gavage， the pathological changes of esophageal tissue and the ultrastructure of ICC were observed. The relative expression and positive expression levels of p62， autophagy-related protein 8 （ATG8）， 200 kDa FAK family kinase-interacting protein （FIP200） and Unc-51 like autophagy activating kinase 1 （ULK1） in esophageal tissue were detected.RESULTS Compared with the blank group， rats in the model group exhibited listlessness； thickening of the esophageal basal layer， elongation of lamina propria papillae with inflammatory cell infiltration； markedly dilated endoplasmic reticulum appearing as round vacuolar cisternae with ribosome detachment； and a small number of accumulated autophagosomes. The relative expression and positive expression levels of p62， ATG8， FIP200， and ULK1 were significantly decreased （ P ＜0.05）. Compared with the model group， the above pathological injuries in the medium- and high-dose Tiaozhong huashi decoction groups had all improved to varying degrees； the damaged endoplasmic reticulum structure was repaired， and no autophagosome accumulation was observed. In particular， the relative expression levels and positive expression levels of p62， ATG8， FIP200， and ULK1 in esophageal tissue of rats in the medium-dose Tiaozhong huashi decoction group were significantly increased （ P ＜0.05）.CONCLUSIONS Tiaozhong huashi decoction ameliorated esophageal mucosal injury in GERD rats， and its mechanism was possibly associated with activation of the p62 signaling pathway and restoration of the endoplasmic reticulum structure， morphology， and autophagic capacity of ICC. |
| 期刊： | 2026年第37卷第19期 |
| 作者： | 滕泽众；陈南；王宇青；罗佐媚；陈广文；黎丽群；刘礼剑；赵雪苹；杨成宁 |
| AUTHORS： | TENG Zezhong，CHEN Nan， WANG Yuqing，LUO Zuomei，CHEN Guangwen，LI Liqun，LIU Lijian，ZHAO Xueping，YANG Chengning |
| 关键字： | 调中化湿汤;胃食管反流病;内质网自噬;p62信号通路;Cajal间质细胞 |
| KEYWORDS： | Tiaozhong huashi decoction;Gastroesophageal reflux disease;endoplasmic reticulum autophagy;p62 signaling pathway;interstitial cells of Cajal |
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