Journal of ethnopharmacology · 2024
Sesquiterpene-enriched extract of Chinese agarwood (Aquilaria sinensis) alleviates bile reflux gastritis through suppression of gastric mucosal cell apoptosis via the Wnt/β-catenin signaling pathway.
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Ma Jiale, Pang Xueping, Xue Weigang, Wang Junjiao, Huo Huixia, Zhao Maoyuan, Huang Yangli, Yin Ziyu, Gao Yun, Zhao Yunfang, Li Jun, Zheng Jiao
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Chinese agarwood (Aquilaria sinensis) has been a traditional treatment for digestive disorders in South and East Asia. While sesquiterpenes are recognized as the key active constituents of Chinese agarwood, the efficacy and mechanism of the sesquiterpene-enriched extract of Chinese agarwood (PEE) on bile reflux gastritis (BRG) remain unclear.
AIM OF THE STUDY: To explore the protective impact of PEE against BRG and unveil its underlying mechanism in suppressing apoptosis of gastric mucosal cells.
MATERIALS AND METHODS: A taurocholic acid (TCA)-induced BRG mouse model was used to assess PEE's protective effects on gastric mucosa histopathology. Transcriptomic analysis was conducted to identify the key signaling pathways affected by PEE. The impact of PEE on apoptosis modulation and Wnt/β-catenin signaling in GES-1 cells was examined. Additionally, the influence of PEE on the Wnt/β-catenin pathway in BRG mouse gastric mucosa was evaluated.
RESULTS: PEE substantially improved gastric tissue damage and inflammation in BRG mice. Transcriptomic analysis revealed that PEE modulates genes linked to apoptosis and the Wnt/β-catenin pathway. In TCA-induced GES-1 cells, PEE enhanced cell viability and mitigated apoptosis via the Wnt/β-catenin pathway, a process potentially mediated by IWP-2, an antagonist of this pathway. Similar regulatory effects were noted in the gastric mucosa of BRG mice.
CONCLUSION: Our research suggests that PEE exerts a protective effect on the gastric tissue through modulating the Wnt/β-catenin pathway to combat apoptosis, which highlights the potential of PEE as a natural remedy for BRG and warrants further investigation into its therapeutic benefits.
AIM OF THE STUDY: To explore the protective impact of PEE against BRG and unveil its underlying mechanism in suppressing apoptosis of gastric mucosal cells.
MATERIALS AND METHODS: A taurocholic acid (TCA)-induced BRG mouse model was used to assess PEE's protective effects on gastric mucosa histopathology. Transcriptomic analysis was conducted to identify the key signaling pathways affected by PEE. The impact of PEE on apoptosis modulation and Wnt/β-catenin signaling in GES-1 cells was examined. Additionally, the influence of PEE on the Wnt/β-catenin pathway in BRG mouse gastric mucosa was evaluated.
RESULTS: PEE substantially improved gastric tissue damage and inflammation in BRG mice. Transcriptomic analysis revealed that PEE modulates genes linked to apoptosis and the Wnt/β-catenin pathway. In TCA-induced GES-1 cells, PEE enhanced cell viability and mitigated apoptosis via the Wnt/β-catenin pathway, a process potentially mediated by IWP-2, an antagonist of this pathway. Similar regulatory effects were noted in the gastric mucosa of BRG mice.
CONCLUSION: Our research suggests that PEE exerts a protective effect on the gastric tissue through modulating the Wnt/β-catenin pathway to combat apoptosis, which highlights the potential of PEE as a natural remedy for BRG and warrants further investigation into its therapeutic benefits.