{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T23:16:34Z","timestamp":1792106194615,"version":"4.4.0"},"reference-count":32,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2024,4,3]],"date-time":"2024-04-03T00:00:00Z","timestamp":1712102400000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Chem Biol Drug Des"],"published-print":{"date-parts":[[2024,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Kaempferol (KPR), a flavonoid compound found in various plants and foods, has garnered attention for its anti\u2010inflammatory, 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)\u2010induced human gallbladder epithelial cells (HGBECs). To assess the impact of KPR on HGBECs, the HGBECs were divided into control, KPR, LPS, LPS\u2009+\u2009KPR, and LPS\u2009+\u2009UDCA groups. Cell viability and cytotoxicity were evaluated by MTT assay and lactate dehydrogenase (LDH) assay, respectively, and concentrations of KPR (10\u2013200\u2009\u03bcM) were tested. LPS\u2010induced inflammatory responses in HGBECs were to create an in\u00a0vitro model of cholecystitis. The key inflammatory markers (IL\u20101\u03b2, IL\u20106, and TNF\u2010\u03b1) levels were quantified using ELISA, The modulation of the MAPK\/NF\u2010\u03baB signaling pathway was measured by western blot using specific antibodies against pathway components (p\u2010I\u03baB\u03b1, I\u03baB\u03b1, p\u2010p65, p65, p\u2010JNK, JNK, p\u2010ERK, ERK, p\u2010p38, and p38). The cell viability and LDH levels in HGBECs were not significantly affected by 50\u2009\u03bcM KPR, thus it was selected as the optimal KPR intervention concentration. KPR increased the viability of LPS\u2010induced HGBECs. Additionally, KPR inhibited the inflammatory factors level (IL\u20101\u03b2, IL\u20106, and TNF\u2010\u03b1) and protein expression (iNOS and COX\u20102) in LPS\u2010induced HGBECs. Furthermore, KPR reversed LPS\u2010induced elevation of p\u2010I\u03baB\u03b1\/I\u03baB\u03b1, p\u2010p65\/p65, p\u2010JNK\/JNK, p\u2010ERK\/ERK, and p\u2010p38\/p38 ratios. KPR attenuates the LPS\u2010induced inflammatory response in HGBECs, possibly by inhibiting MAPK\/NF\u2010\u03baB signaling.<\/jats:p>","DOI":"10.1111\/cbdd.14519","type":"journal-article","created":{"date-parts":[[2024,4,3]],"date-time":"2024-04-03T23:13:55Z","timestamp":1712186035000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Kaempferol attenuates inflammation in lipopolysaccharide\u2010induced gallbladder epithelial cells by inhibiting the\n                    <scp>MAPK<\/scp>\n                    \/\n                    <scp>NF\u2010\u03baB<\/scp>\n                    signaling pathway"],"prefix":"10.1111","volume":"103","author":[{"given":"Hai\u2010tao","family":"Wu","sequence":"first","affiliation":[{"name":"Department of General Surgery Dafeng People's Hospital  Yancheng Jiangsu 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