Journal of inflammation research · 2025
Jianpi Lishi Jiedu Decoction (JLJD) Inhibit Th17 Cell Differentiation via the Jak/Stat3/RORγt Pathway in Colorectal Adenomas.
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Si Min, Wang Yan, Wu Hao, Huang Yuzhen, Ma Mengqing, Su Kunhan, Qiao Dan, Tao Weiwei, Liu Wanli
Аннотация
BACKGROUND: Jianpi Lishi Jiedu Decoction (JLJD) are used in China to prevent colorectal adenoma recurrence, but their molecular mechanism is unclear.
OBJECTIVE: Evaluate JLJD's preventive and therapeutic effects on colorectal adenomas and elucidate its molecular mechanisms.
METHODS: JLJD components were identified via HPLC. The Apc Min/+ mouse model assessed therapeutic efficacy. Effects on colorectal tissue proliferation/apoptosis were analyzed. Flow cytometry evaluated Th17 cells; ELISA quantified inflammatory cytokines (IL-17, IL-6, IL-1β, IL-18). Jak2/Stat3/RORγt pathway proteins were detected by Western blot (WB) and immunohistochemistry (IHC). A Jak2 activator (RO8191) validated functional targets. Key components (chlorogenic acid, atractylenolide I) were tested in vitro for: (1) non-toxic concentrations (MTT), (2) IL-17A levels, (3) Th17 differentiation, (4) p-Stat3/RORγt expression (WB).
RESULTS: JLJD significantly reduced adenoma number and progression in Apc Min/+ mice. Anti-Ki67 IHC showed suppressed proliferation; TUNEL assay confirmed induced apoptosis. ELISA indicated JLJD significantly decreased pro-inflammatory cytokine levels. WB/IHC demonstrated JLJD inhibited Th17 cell differentiation by downregulating Jak2/Stat3/RORγt pathway proteins in colon tissues and mesenteric lymph nodes. RO8191 abrogated JLJD's anti-adenoma effects, reversed Th17 suppression, and nullified pathway inhibition. In vitro, chlorogenic acid and atractylenolide I significantly reduced IL-17A, reversed Th17 expansion, and decreased p-Stat3/RORγt expression.
CONCLUSION: JLJD inhibits the differentiation of Th17 cells by suppressing the Jak2/Stat3/RORγ pathway, thereby exerting an inhibitory effect on colorectal adenomas.
OBJECTIVE: Evaluate JLJD's preventive and therapeutic effects on colorectal adenomas and elucidate its molecular mechanisms.
METHODS: JLJD components were identified via HPLC. The Apc Min/+ mouse model assessed therapeutic efficacy. Effects on colorectal tissue proliferation/apoptosis were analyzed. Flow cytometry evaluated Th17 cells; ELISA quantified inflammatory cytokines (IL-17, IL-6, IL-1β, IL-18). Jak2/Stat3/RORγt pathway proteins were detected by Western blot (WB) and immunohistochemistry (IHC). A Jak2 activator (RO8191) validated functional targets. Key components (chlorogenic acid, atractylenolide I) were tested in vitro for: (1) non-toxic concentrations (MTT), (2) IL-17A levels, (3) Th17 differentiation, (4) p-Stat3/RORγt expression (WB).
RESULTS: JLJD significantly reduced adenoma number and progression in Apc Min/+ mice. Anti-Ki67 IHC showed suppressed proliferation; TUNEL assay confirmed induced apoptosis. ELISA indicated JLJD significantly decreased pro-inflammatory cytokine levels. WB/IHC demonstrated JLJD inhibited Th17 cell differentiation by downregulating Jak2/Stat3/RORγt pathway proteins in colon tissues and mesenteric lymph nodes. RO8191 abrogated JLJD's anti-adenoma effects, reversed Th17 suppression, and nullified pathway inhibition. In vitro, chlorogenic acid and atractylenolide I significantly reduced IL-17A, reversed Th17 expansion, and decreased p-Stat3/RORγt expression.
CONCLUSION: JLJD inhibits the differentiation of Th17 cells by suppressing the Jak2/Stat3/RORγ pathway, thereby exerting an inhibitory effect on colorectal adenomas.