Endocrine, metabolic & immune disorders drug targets · 2026
Palmatine Ameliorates High-Temperature and High-Humidity-Induced Enteritis via Mitophagy and NLRP3 Inflammasome Degradation.
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Mo Xiaoying, Mi Tai, Liu Wanli, Wang Yao, Wu Yalan, Huang Xinhua, Chen Song, Luo Huanhuan
Аннотация
BACKGROUND: Previous studies have shown that a High-Temperature- and High-Humidity (HTH) environment leads to mild enteritis, accompanied by impaired mitophagy and activated NLRP3-IL-1β, as found in Inflammatory Bowel Disease (IBD). Therefore, whether Palmatine (PAL), a candidate for treating IBD, ameliorates HTH-induced enteritis via mitophagy-associated mechanisms was examined. This study aimed to investigate the protective effects of PAL against HTH-induced enteritis in mice and determine the underlying mechanisms.
METHODS: BALB/c mice were used to model HTH-induced enteritis. The mice were exposed to an HTH environment (33 ± 0.5°C, 85-90% humidity) for 28 days, with PAL or Cyclosporin A (CsA) administered daily. Mice were euthanized on days 7, 14, 28, or 35 to analyze the ileal tissues. Pathological examination, western blotting (Parkin, NLRP3, IL-1β), immunofluorescence (8-OHDG), and mtDNA quantification were performed to assess the therapeutic effects of the treatment.
RESULTS: A total of 884 and 2,668 potential targeted genes were identified for PAL and IBD, respectively, including 183 overlapped genes, which were mainly involved in oxidative stress, inflammation, and autophagy. HTH induced weight loss and loose faeces, along with increased NLRP3, IL-1β, and 8-OHDG expressions, and decreased Parkin and mtDNA expressions in the ileum. These effects were ameliorated and exacerbated by PAL and CsA treatment, respectively.
DISCUSSION: Palmatine ameliorates HTH-induced enteritis by regulating the mitophagy-NLRP3 inflammasome axis. It activates Parkin-mediated mitophagy, increasing mtDNA copy number, reducing mtROS and 8-OHDG, thereby inhibiting NLRP3 inflammasome activation and IL-1β secretion. CsA reversed these effects, confirming the mitophagy-dependent mechanism. The safe dosage supports its therapeutic potential against environment-related intestinal inflammation.
CONCLUSION: PAL ameliorated HTH-induced enteritis probably via augmenting mitophagy and in hibiting NLRP3 expression. The findings highlight the critical role of mitophagy in the pathogenesis of HTH-induced enteritis and support the potential use of PAL in treatment.
METHODS: BALB/c mice were used to model HTH-induced enteritis. The mice were exposed to an HTH environment (33 ± 0.5°C, 85-90% humidity) for 28 days, with PAL or Cyclosporin A (CsA) administered daily. Mice were euthanized on days 7, 14, 28, or 35 to analyze the ileal tissues. Pathological examination, western blotting (Parkin, NLRP3, IL-1β), immunofluorescence (8-OHDG), and mtDNA quantification were performed to assess the therapeutic effects of the treatment.
RESULTS: A total of 884 and 2,668 potential targeted genes were identified for PAL and IBD, respectively, including 183 overlapped genes, which were mainly involved in oxidative stress, inflammation, and autophagy. HTH induced weight loss and loose faeces, along with increased NLRP3, IL-1β, and 8-OHDG expressions, and decreased Parkin and mtDNA expressions in the ileum. These effects were ameliorated and exacerbated by PAL and CsA treatment, respectively.
DISCUSSION: Palmatine ameliorates HTH-induced enteritis by regulating the mitophagy-NLRP3 inflammasome axis. It activates Parkin-mediated mitophagy, increasing mtDNA copy number, reducing mtROS and 8-OHDG, thereby inhibiting NLRP3 inflammasome activation and IL-1β secretion. CsA reversed these effects, confirming the mitophagy-dependent mechanism. The safe dosage supports its therapeutic potential against environment-related intestinal inflammation.
CONCLUSION: PAL ameliorated HTH-induced enteritis probably via augmenting mitophagy and in hibiting NLRP3 expression. The findings highlight the critical role of mitophagy in the pathogenesis of HTH-induced enteritis and support the potential use of PAL in treatment.