Bruguiera gymnorrhiza (L.) Lam. Fruit Accelerates Healing in Gastric Injury via the Regulation of the NF-κB Pathway.

Objective: The present study aimed at the anti-inflammatory and antioxidant effects of the extract of Bruguiera gymnorrhiza (L.) Lam. fruit (BGF) on the gastric injury. Materials and Methods: The chemical components in the extract of BGF were used in UPLC/Q-Orbitrap analysis. 60 SD rats were randomized into six groups: normal group (MC), ethanol-injured control group (EC), omeprazole group, and three groups with different doses (50, 100, and 200 mg/kg) of BGF. After continuous administration for seven days, the stomachs of rats were taken out to observe the pathological gastric tissue changes; inflammatory factors and oxidative stress markers in the stomach tissues were measured. Western blot (WB) analyses were conducted to explore the mechanism of BGF on gastric tissue and RAW 246.7 cells with excessive inflammation. Results: BGF enhanced gastric mucosal protection by improving the mucosal blood flow of the stomach and significantly decreased inflammatory factors and oxidative stress markers. Moreover, BGF significantly reduced the expression of p-NF-κB p65. Consistently, BGF demonstrated similar effects on LPS-induced RAW 264.7 cells as it did in vivo. Conclusion: BGF could accelerate the healing of gastric injury by exerting antioxidant and anti-inflammatory effects and maintaining mucosal integrity.

Metabolomics and integrated network pharmacology analysis reveal attenuates cardiac hypertrophic mechanisms of HuoXin pill.

ETHNOPHARMACOLOGICAL RELEVANCE: Cardiac hypertrophy (CH) is maladaptive and contributes to the pathogenesis of heart failure. Huoxin pill (HXP), a Chinese herbal prescription, is widely applied in the treatment of cardiovascular disease (CAD). Its mechanism, however, is unclear. AIM OF THE STUDY: This study investigated the mechanism of action for Huoxin pill in the treatment of CH, an important stage of CAD. MATERIALS AND METHODS: A total of 60 rats were injected with isoprenaline (ISO) to establish a model of CH. Echocardiography and histopathologic evaluation were performed to evaluate the disease severity, whereas ELISAs were conducted to determine the expression of oxidative stress. Network pharmacology and metabolomic analyses were conducted to identify the key compounds, core targets and pathways that mediate the effects of HXP against CH. Western blotting and immunohistochemistry were used to test apoptosis protein levels. RESULTS: HXP administration in ISO-treated rats decreased hypertrophy indices, alleviated cardiac pathological damage, and downregulated oxidative stress levels when compared to those of rats subjected to ISO treatment only. Moreover, network pharmacology results suggested that the PI3K-Akt pathway is a main mechanism by which HXP inhibits cardiac hypertrophy, and experimental verification showed that HXP inhibited cardiomyocyte apoptosis via activation of the PI3K-Akt pathway. The results of metabolomic analysis identified 21 differential metabolites between the HXPH group and ISO group, which were considered to be metabolic biomarkers of HXP in the treatment of CH. Among them, 6 differential metabolites were significantly upregulated, and 15 were significantly downregulated. CONCLUSIONS: The present study presents an integrated strategy for investigating the mechanisms of HXP in the treatment of CH and sheds new light on the application of HXP as a traditional Chinese medicine.