Kangfuxin solution alleviates esophageal stenosis after endoscopic submucosal dissection:A natural ingredient strategy  

作　　者：Xin Zhou Dan Ma Yi-Xiang He Jing Jin Hong-Lian Wang Yun-Feng Wang Fan Yang Jian-Qin Liu Jie Chen Zhi Li 

机构地区：[1]Department of Spleen and Stomach Diseases,the Affiliated Traditional Chinese Medicine Hospital,Southwest Medical University,Luzhou 646000,Sichuan Province,China [2]The Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Digestive System Diseases of Luzhou City,The Affiliated Traditional Medicine Hospital,Southwest Medical University,Luzhou 646000,Sichuan Province,China [3]Department of Gastroenterology,Changhai Hospital,Naval Medical University,Shanghai 20082,China [4]Research Center of Integrated Chinese and Western Medicine,The Affiliated Traditional Chinese Medicine Hospital,Southwest Medical University,Luzhou 646000,Sichuan Province,China [5]School of Integrated Traditional Chinese and Western Clinical Medicine,North Sichuan Medical College,Nanchong,637100,Sichuan Province,China

出　　处：《World Journal of Gastroenterology》2025年第1期110-125,共16页世界胃肠病学杂志（英文）

基　　金：Supported by Science and Technology Department of Sichuan Province,No.2020YFS0376;National Natural Science Foundation of China,No.81900599;Science and Technology Program of Hospital of TCM,Southwest Medical University,No.2022-CXTD-01.

摘　　要：BACKGROUND Esophageal stricture ranks among the most significant complications following endoscopic submucosal dissection(ESD).Excessive fibrotic repair is a typical pathological feature leading to stenosis after ESD.AIM To examine the effectiveness and underlying mechanism of Kangfuxin solution(KFX)in mitigating excessive fibrotic repair of the esophagus post-ESD.METHODS Pigs received KFX at 0.74 mL/kg/d for 21 days after esophageal full circumferential ESD.Endoscopic examinations occurred on days 7 and 21 post-ESD.In vitro,recombinant transforming growth factor(TGF)-β1(5 ng/mL)induced a fibrotic microenvironment in primary esophageal fibroblasts(pEsF).After 24 hours of KFX treatment(at 1.5%,1%,and 0.5%),expression ofα-smooth muscle actin-2(ACTA2),fibronectin(FN),and type collagen I was assessed.Profibrotic signaling was analyzed,including TGF-β1,Smad2/3,and phosphor-smad2/3(p-Smad2/3).RESULTS Compared to the Control group,the groups treated with KFX and prednisolone exhibited reduced esophageal stenosis,lower weight loss rates,and improved food tolerance 21 d after ESD.After treatment,Masson staining revealed thinner and less dense collagen fibers in the submucosal layer.Additionally,the expression of fibrotic effector molecules was notably inhibited.Mechanistically,KFX downregulated the transduction levels of fibrotic functional molecules such as TGF-β1,Smad2/3,and p-Smad2/3.In vitro,pEsF exposed to TGF-β1-induced fibrotic microenvironment displayed increased fibrotic activity,which was reversed by KFX treatment,leading to reduced activation of ACTA2,FN,and collagen I.The 1.5%KFX treatment group showed decreased expression of p-Smad 2/3 in TGF-β1-activated pEsF.CONCLUSION KFX showed promise as a therapeutic option for post-full circumferential esophageal ESD strictures,potentially by suppressing fibroblast fibrotic activity through modulation of the TGF-β1/Smads signaling pathway.

关 键 词：Kangfuxin solution Natural component Endoscopic submucosal dissection Esophagus stricture Fibrosis 

分 类 号：R735.34[医药卫生—肿瘤]