Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Bioactive compound emodin from clinical formula Zhi-Lou-Xun-Xi decoction exerts rapid analgesic effects by targeting TRPV1.
СтатьяНазвание и аннотация: Перевод в очереди
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Chen Chen, Jin Zecheng, Qiu Zhengxi, Chen Zepeng, Zhou Jin-Yong, Hou Wei, Bu Zhijun, Yao Shuang, Ma Yimeng, Yin Hongye, Ma Jiaze, Cao Xia, Wang Juejin, Zhang Yinan, Chen Yugen
Аннотация
BACKGROUND: Effective postoperative pain management after hemorrhoidectomy remains a significant clinical challenge, largely due to the scarcity of safe and effective non-opioid analgesics. Zhi-Lou-Xun-Xi decoction (J5) is a traditional Chinese formula that has been used clinically for decades, yet its active components and mechanism of action remain unclear.
PURPOSE: This study aimed to systematically identify the active analgesic components in J5 and elucidate their molecular mechanism of action.
METHODS: We employed an integrated pharmacological approach, beginning with a retrospective clinical analysis to confirm the analgesic and wound-healing effects of J5. Pharmacodynamic assays were conducted to evaluate its interaction with TRPV1. High-resolution mass spectrometry and structure-based virtual screening were used to identify candidate compounds. The mechanism of emodin, the primary active constituent, was further investigated through SPR assays, patch-clamp recording, molecular dynamics simulations, and extensive in vivo pain models using TRPV1 knockout (KO) mice.
RESULTS: Emodin was identified as the key TRPV1-antagonizing component in J5. In multiple pain models, emodin produced dose-dependent analgesia without inducing common TRPV1 antagonist-related side effects, particularly altered thermal sensitivity or hyperthermia. These findings not only clarify the mechanistic basis of J5's clinical efficacy but also position emodin as a promising topical analgesic candidate that acts via local TRPV1 inhibition.
PURPOSE: This study aimed to systematically identify the active analgesic components in J5 and elucidate their molecular mechanism of action.
METHODS: We employed an integrated pharmacological approach, beginning with a retrospective clinical analysis to confirm the analgesic and wound-healing effects of J5. Pharmacodynamic assays were conducted to evaluate its interaction with TRPV1. High-resolution mass spectrometry and structure-based virtual screening were used to identify candidate compounds. The mechanism of emodin, the primary active constituent, was further investigated through SPR assays, patch-clamp recording, molecular dynamics simulations, and extensive in vivo pain models using TRPV1 knockout (KO) mice.
RESULTS: Emodin was identified as the key TRPV1-antagonizing component in J5. In multiple pain models, emodin produced dose-dependent analgesia without inducing common TRPV1 antagonist-related side effects, particularly altered thermal sensitivity or hyperthermia. These findings not only clarify the mechanistic basis of J5's clinical efficacy but also position emodin as a promising topical analgesic candidate that acts via local TRPV1 inhibition.