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Sweet (\n                    <jats:italic>Clerodendrum japonicum<\/jats:italic>\n                    ) is a traditional medicinal plant with reported anti\u2010inflammatory use, but its anti\u2010rheumatoid arthritis (RA) activity and molecular basis remain insufficiently characterized. Activated fibroblast\u2010like synoviocytes (FLSs) contribute to persistent inflammation and joint destruction in rheumatoid arthritis (RA). This study investigated whether extracts of\n                    <jats:italic>Clerodendrum japonicum<\/jats:italic>\n                    attenuate pathogenic RA\u2010FLS phenotypes and examined the possible involvement of METTL3\u2010dependent N6\u2010methyladenosine (m6A) regulation of ICAM2 mRNA. Tumor necrosis factor\u2010\u03b1\u2010stimulated human RA\u2010FLSs (MH7A cell line) were used as an in vitro model to evaluate the anti\u2010RA effects of\n                    <jats:italic>Clerodendrum japonicum<\/jats:italic>\n                    extracts. Cell proliferation, apoptosis, migration, invasion, and inflammatory cytokine secretion were evaluated. The underlying mechanisms were further investigated using real\u2010time quantitative polymerase chain reaction, Western blot, and RNA immunoprecipitation. In addition, a collagen\u2010induced arthritis (CIA) mouse model was employed to validate the anti\u2010RA effects of the extracts\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Drug\u2010containing serum derived from\n                    <jats:italic>Clerodendrum japonicum<\/jats:italic>\n                    extracts attenuated TNF\u2010\u03b1\u2010induced proliferation, migration, invasion, and pro\u2010inflammatory cytokine release in MH7A cells while increasing apoptosis. The ethyl acetate fraction (CJEA) produced the most pronounced effects among the tested fractions. CJEA\u2010containing serum reduced global m6A abundance and METTL3 expression. METTL3 overexpression partially reversed the cellular effects associated with CJEA\u2010containing serum. METTL3 knockdown reduced m6A enrichment and stability of ICAM2 mRNA, whereas METTL3 or ICAM2 overexpression partially restored ICAM2 expression and pathogenic RA\u2010FLS phenotypes. Oral CJEA also reduced clinical and histological arthritis severity in CIA mice and was associated with lower synovial METTL3 and ICAM2 expression. Our findings support the involvement of METTL3\u2010dependent m6A regulation of ICAM2 mRNA in the response of RA\u2010FLSs to CJEA\u2010containing serum. CJEA may attenuate pathogenic RA\u2010FLS behavior and experimental arthritis at least partly through modulation of this pathway. Because the active constituent(s), direct molecular target, pharmacokinetics, and comprehensive safety profile remain undefined, further chemical and pharmacological validation is required.\n                  <\/jats:p>","DOI":"10.1002\/cbf.70303","type":"journal-article","created":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:50:58Z","timestamp":1789973458000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<i>Clerodendrum japonicum<\/i>\n                    Extract Suppresses the Pathogenicity of Rheumatoid Arthritis Fibroblast\u2010Like Synoviocytes by Inhibiting METTL3\u2010Mediated ICAM2 mRNA Methylation"],"prefix":"10.1002","volume":"44","author":[{"given":"Ying","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Gynecology International Zhuang Medicine Hospital Affiliated to Guangxi University of Chinese Medicine Nanning City Guangxi Zhuang Autonomous Region 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