Preventive effects of traditional Chinese medicine formula Huoxiangzhengqi against lipopolysaccharide-induced inflammatory response

• Published in: Phytomedicine (Stuttgart) 2022-05, Vol.99, p.153968, Article 153968
• Main Authors: Gao, Min, Zou, Zhen, Qiu, Yu, Sumayyah, Golamaully, Jiang, Xuejun, Su, Junhao, Duan, Xinhao, Chen, Chengzhi, Qiu, Jingfu
• Format: Article
• Language: English
• Subjects: Gut microbiota; Huoxiangzhengqi; Inflammation; Lipopolysaccharide
• ISSN: 0944-7113; 1618-095X
• DOI: 10.1016/j.phymed.2022.153968

•Pretreatment with HX ameliorated intestinal damage caused by LPS.•Pretreatment with HX alleviated LPS-induced intestinal and brain inflammation.•Pretreatment with HX prevented LPS-induced alterations of NF-κB signaling pathway.•Pretreatment with HX did not affect the LPS-induced imbalance of gut microbiota.•Pretreatment with HX partially affected the levels of gut-brain peptides. Huoxiangzhengqi oral liquid (HX), a pharmaceutical product made from traditional Chinese medicine formulas, has been commonly used in household medication for gastrointestinal disorders, but the mode of action remains largely unclear. This study aims to investigate whether pretreatment with HX prevents lipopolysaccharide (LPS)-induced adverse effects and the potential mechanisms involved. Seven-week-old male C57BL/6J mice were orally administered low (1.3 ml/kg) and high doses (2.6 ml/kg) of HX for 7 days, and subsequently subjected to a single dose of LPS at 6 mg/kg. Dexamethasone served as the positive control. Each group had ten animals. The data demonstrated that either a low or high dose of HX significantly reduced the levels of inflammation induced by LPS in both small intestinal and cortical tissues. LPS profoundly decreased the richness and evenness of the microbiota and disrupted the composition of the intestinal microbial community, but pretreatment with HX did not successfully prevent dysbiosis. No significant improvements in HX against LPS were observed in intestinal local immunity or the secretion of partial gut-brain peptides. In addition, pretreatment with HX prevented the alterations in the expression levels of proteins related to the NF-κB pathway, including phospho-p38, p38, phospho-p44/42, p44/42, p50 and p65 induced by LPS. Herein, we demonstrated for the first time that the preventive effects of HX against LPS mainly occur through the inhibition of inflammation. These findings provide novel evidence that HX may serve as a new agent for the prevention of gastrointestinal inflammation-related disorders. [Display omitted]