Zheng Xiaoying, Zhang Shuning, Chen Qiaobin
Department of Pediatrics, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, No. 134 Dong Street, Fuzhou, Fujian, 350001, China.
Major of Pediatrics, Fujian Medical University, Fuzhou, Fujian, 350001, China.
Open Life Sci. 2025 Jan 27;20(1):20221036. doi: 10.1515/biol-2022-1036. eCollection 2025.
Functional dyspepsia (FD) is a chronic disease that occurs in the gastroduodenal region and significantly impacts human health. Maslinic acid (MA), a pentacyclic triterpene acid, is the primary bioactive ingredient in Chinese medicinal herbs such as hawthorn, which exhibits beneficial impacts on the regulation of various disease progressions. However, the specific functions and associated pathways of MA in FD progression remain unclear and require further investigation. In this work, it was demonstrated that MA enhanced the cell viability of human gastric smooth muscle cells (HGSMCs). In addition, the mitochondrial dysfunctions induced by carbonyl cyanide 3-chlorophenylhydrazone (CCCP) were rescued after MA treatment. Furthermore, autophagy was increased following CCCP treatment, but this phenomenon was counteracted after MA treatment. The oxidative stress, elevated after CCCP treatment, was alleviated following MA addition. Finally, the AMPK/SIRT1 pathway was suppressed after CCCP stimulation but was re-activated after MA treatment. In conclusion, it was uncovered that MA accelerated HGSMC viability and improved mitochondrial function, inhibited autophagy, alleviated oxidative stress, and stimulated the AMPK/SIRT1 pathway. This discovery may offer new insight into the therapeutic effects of MA in FD progression.
功能性消化不良（FD）是一种发生在胃十二指肠区域的慢性疾病，对人类健康有重大影响。齐墩果酸（MA）是一种五环三萜酸，是山楂等中药材中的主要生物活性成分，对多种疾病进程的调节具有有益作用。然而，MA在FD进展中的具体功能和相关途径仍不清楚，需要进一步研究。在这项研究中，证明了MA增强了人胃平滑肌细胞（HGSMC）的细胞活力。此外，MA处理后挽救了由羰基氰3-氯苯腙（CCCP）诱导的线粒体功能障碍。此外，CCCP处理后自噬增加，但MA处理后这种现象被抵消。CCCP处理后升高的氧化应激在添加MA后得到缓解。最后，CCCP刺激后AMPK/SIRT1途径被抑制，但MA处理后重新激活。总之，发现MA加速了HGSMC活力，改善了线粒体功能，抑制了自噬，减轻了氧化应激，并刺激了AMPK/SIRT1途径。这一发现可能为MA在FD进展中的治疗作用提供新的见解。
