Kaempferol attenuates inflammation in lipopolysaccharide‐induced gallbladder epithelial cells by inhibiting the MAPK/NF‐κB signaling pathway

Abstract

AbstractKaempferol (KPR), a flavonoid compound found in various plants and foods, has garnered attention for its anti‐inflammatory, antioxidant, and anticancer properties. In preliminary studies, KPR can modulate several signaling pathways involved in inflammation, making it a candidate for treating cholecystitis. This study aimed to explore the effects and mechanisms of KPR on lipopolysaccharide (LPS)‐induced human gallbladder epithelial cells (HGBECs). To assess the impact of KPR on HGBECs, the HGBECs were divided into control, KPR, LPS, LPS + KPR, and LPS + UDCA groups. Cell viability and cytotoxicity were evaluated by MTT assay and lactate dehydrogenase (LDH) assay, respectively, and concentrations of KPR (10–200 μM) were tested. LPS‐induced inflammatory responses in HGBECs were to create an in vitro model of cholecystitis. The key inflammatory markers (IL‐1β, IL‐6, and TNF‐α) levels were quantified using ELISA, The modulation of the MAPK/NF‐κB signaling pathway was measured by western blot using specific antibodies against pathway components (p‐IκBα, IκBα, p‐p65, p65, p‐JNK, JNK, p‐ERK, ERK, p‐p38, and p38). The cell viability and LDH levels in HGBECs were not significantly affected by 50 μM KPR, thus it was selected as the optimal KPR intervention concentration. KPR increased the viability of LPS‐induced HGBECs. Additionally, KPR inhibited the inflammatory factors level (IL‐1β, IL‐6, and TNF‐α) and protein expression (iNOS and COX‐2) in LPS‐induced HGBECs. Furthermore, KPR reversed LPS‐induced elevation of p‐IκBα/IκBα, p‐p65/p65, p‐JNK/JNK, p‐ERK/ERK, and p‐p38/p38 ratios. KPR attenuates the LPS‐induced inflammatory response in HGBECs, possibly by inhibiting MAPK/NF‐κB signaling.