Journal of ethnopharmacology · 2026
Dual benefits of Xiao Chai Hu Tang and its active compounds in CPT-11 therapy: intestinal protection via barrier restoration and anti-inflammation combined with enhanced tumor apoptosis.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhang Yangyang, Cao Xia, Hou Zong, Liu Zhiqiang, Liu Shu
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Xiao Chai Hu Tang (XCHT) is a classic Chinese herbal formula traditionally used for gastrointestinal disorders. Although XCHT alleviates irinotecan (CPT-11)-induced diarrhea, whether it confers the dual benefit of concurrently reducing intestinal toxicity and enhancing antitumor apoptosis remains unknown.
AIM OF THE STUDY: To determine whether XCHT confers dual benefits in CPT-11-treated colorectal cancer (CRC), elucidate the underlying mechanisms, and identify the active constituents responsible.
MATERIALS AND METHODS: A DMH/DSS-induced CRC rat model was established to evaluate XCHT in CPT-11 therapy. Intestinal barrier integrity, inflammation, and tumor apoptosis were assessed. Effects were validated in SN-38-treated NCM-460 (barrier protection, anti-inflammation) and HCT-116 cells (synergistic apoptosis). Systemically absorbed constituents were identified by HPLC-Q-Orbitrap MS and functionally validated.
RESULTS: XCHT mitigated CPT-11-induced toxicity in CRC rats by restoring tight junction proteins (ZO-1, occludin) and suppressing NLRP3 inflammasome-mediated inflammation (IL-1β, IL-18, IL-6, TNF-α), with these effects recapitulated in SN-38-treated NCM-460 cells. XCHT also enhanced CPT-11-induced apoptosis in tumor tissues and synergized with SN-38 in HCT-116 cells, as evidenced by increased Bax/Bcl-2 ratio. Among 17 systemically absorbed compounds, baicalein, baicalin, and wogonin were identified as key contributors to barrier protection and anti-inflammation, while baicalein and isoliquiritin were associated with the synergistic pro-apoptotic effect with SN-38 in functional screening.
CONCLUSION: XCHT improves CPT-11's therapeutic index by protecting intestinal barrier, suppressing NLRP3 inflammasome, and enhancing tumor apoptosis through distinct bioactive constituents. These findings provide a pharmacochemical and mechanistic foundation for its adjunctive use in CRC treatment.
AIM OF THE STUDY: To determine whether XCHT confers dual benefits in CPT-11-treated colorectal cancer (CRC), elucidate the underlying mechanisms, and identify the active constituents responsible.
MATERIALS AND METHODS: A DMH/DSS-induced CRC rat model was established to evaluate XCHT in CPT-11 therapy. Intestinal barrier integrity, inflammation, and tumor apoptosis were assessed. Effects were validated in SN-38-treated NCM-460 (barrier protection, anti-inflammation) and HCT-116 cells (synergistic apoptosis). Systemically absorbed constituents were identified by HPLC-Q-Orbitrap MS and functionally validated.
RESULTS: XCHT mitigated CPT-11-induced toxicity in CRC rats by restoring tight junction proteins (ZO-1, occludin) and suppressing NLRP3 inflammasome-mediated inflammation (IL-1β, IL-18, IL-6, TNF-α), with these effects recapitulated in SN-38-treated NCM-460 cells. XCHT also enhanced CPT-11-induced apoptosis in tumor tissues and synergized with SN-38 in HCT-116 cells, as evidenced by increased Bax/Bcl-2 ratio. Among 17 systemically absorbed compounds, baicalein, baicalin, and wogonin were identified as key contributors to barrier protection and anti-inflammation, while baicalein and isoliquiritin were associated with the synergistic pro-apoptotic effect with SN-38 in functional screening.
CONCLUSION: XCHT improves CPT-11's therapeutic index by protecting intestinal barrier, suppressing NLRP3 inflammasome, and enhancing tumor apoptosis through distinct bioactive constituents. These findings provide a pharmacochemical and mechanistic foundation for its adjunctive use in CRC treatment.