结肠镜引导下消痔灵硬化剂注射治疗内痔93例疗效观察

目的：观察结肠镜引导下消痔灵硬化剂注射治疗内痔的疗效及安全性。方法：选取93例Ⅰ～Ⅲ期内痔患者为观察对象,均采用结肠镜引导下消痔灵注射液内痔注射治疗,观察治疗后临床疗效和并发症情况。结果：93例患者治疗后出血和脱出评分均优于治疗前（P <0.001）,总有效率为91.40%。术后7d内发生肛门坠胀37例（39.78%）,肛门疼痛6例（6.45%）,术后1个月内发生肛门狭窄1例（1.08%）,无尿潴留、肛周感染、肛门失禁及消化道大出血发生。结论：结肠镜引导下消痔灵注射治疗内痔是一种安全、有效的方法,值得临床推广应用。     

华蟾素对溃疡性结肠炎大鼠的作用及机制北大核心CSCD

目的研究华蟾素对溃疡性结肠炎(UC)大鼠的作用及其机制。方法用2,4,6-三硝基苯磺酸(TNBS)结肠灌注建立UC大鼠模型。按照大鼠体重随机分为对照组、模型组、阳性对照组、华蟾素低剂量组(HCS-L)、华蟾素高剂量组(HCS-H),每组6只。对照组、模型组予以生理盐水灌肠,阳性对照组给予美沙拉嗪灌肠液1.5 g·kg^(-1)灌肠,HCS-L、HCS-H分别予以华蟾素200、400 mg·kg^(-1)灌肠,每日1次,连续14 d。用疾病活动指数(DAI)、结肠黏膜损伤指数(CMDI)进行评分,用苏木素-伊红(HE)染色观察结肠病理变化,用酶联免疫吸附(ELISA)法检测血清中炎性因子水平,用免疫组化法检测结肠组织中NOD样受体蛋白3(NLRP3)、胱天蛋白酶-1(caspase-1)、咬合蛋白(Occludin)、带状闭合蛋白(ZO-1)的表达情况。结果对照组、模型组、阳性对照组、HCS-L、HCS-H的DAI评分分别为0.11±0.27,2.44±0.54,1.22±0.78,1.33±0.73,1.06±0.61;上述5组的CMDI评分分别为0.17±0.41,2.83±1.17,1.00±0.89,1.33±0.52,0.83±0.75;与正常组比较,模型组DAI评分、CMDI评分均显著升高,与模型组比较,阳性对照组、HCS-L、HCS-H的DAI评分、CMDI评分均显著降低(均P<0.05)。与正常组比较,模型组血清中白细胞介素-1β(IL-1β)、白细胞介素-18(IL-18)、肿瘤坏死因子-α(TNF-α)均显著升高,与模型组比较,阳性对照组、HCS-L、HCS-H血清中IL-1β、IL-18、TNF-α均显著降低(均P<0.01);与正常组比较,模型组结肠组织中NLRP3、caspase-1的平均光密度值均显著升高,Occludin、ZO-1的平均光密度值均显著降低(均P<0.01),与模型组比较,阳性对照组、HCS-L、HCS-H结肠组织中NLRP3、casepase-1的平均光密度值均显著降低,Occludin、ZO-1的平均光密度值均显著升高(均P<0.01)。结论华蟾素可明显缓解UC大鼠症状,改善UC大鼠肠黏膜病变,其机制可能与抑制NLRP3的过度激活、降低炎症反应、增强黏膜屏障的完整性有关。     

华蟾素对FOLFOX化疗小鼠肠道炎症及黏膜屏障的影响

目的 观察华蟾素对FOLFOX化疗小鼠肠道炎症及黏膜屏障的影响,探讨华蟾素缓解化疗相关性腹泻(CID)的机制.方法 将28只BALB/c小鼠随机分为4组:正常组,FOLFOX组,华蟾素低剂量组(260 mg·kg-1),华蟾素高剂量组(520 mg·kg-1).FOLFOX组予以FOLFOX化疗方案连续腹腔注射5 d,...     

结直肠肿瘤术后吻合口狭窄的内镜下切开扩张治疗

目的:探讨内镜下切开扩张术治疗结直肠肿瘤术后吻合口狭窄的临床疗效。方法:选取2019年2月至2022年2月，西南医科大学附属中医医院26例结直肠肿瘤术后吻合口良性狭窄患者，采用内镜下切开扩张术治疗，术后进行疗效评价及随访。结果:26例患者中，痊愈19例，好转3例，无效4例。无效患者经5次以上的切开扩张治疗后仍反复狭窄。围手术期均未出现严重并发症。19例痊愈患者中，治疗后吻合口直径明显增大，约12.0 mm～15.0 mm,肠镜可顺利通过。3例好转患者需反复多次的内镜下切开扩张治疗。治疗后随访3～6个月，19例患者均未再出现严重狭窄，未再出现排便困难、肠梗阻及腹痛等。结论:内镜下切开扩张治疗结直肠肿瘤术后吻合口狭窄安全有效。     

基于网络药理学和分子对接研究华蟾素治疗胃癌的作用机制

目的 基于网络药理学和分子对接研究华蟾素治疗胃癌的作用机制。方法 通过药物靶点预测网站获得华蟾素成分靶点，疾病数据库获取胃癌疾病基因，将两者共同靶点进行GO功能富集分析及KEGG通路分析，Cytoscape软件构建蛋白互作(PPI)网络和药物-靶点-疾病相互作用网络。通过Kaplan-Meier分析关键靶点与胃癌预后的相关性，分子对接分析华蟾素成分与关键靶点的结合情况，最后筛选出核心靶点，并通过TCGA、GEO数据库进行单因素、多因素Cox回归分析以验证其与胃癌预后的关系。结果 华蟾素治疗胃癌涉及70个靶点、1 399个生物学过程、75个分子功能、145条信号通路，通过药物-靶点-疾病相互作用网络筛选出关键化合物5个、关键靶点10个，其中与胃癌预后相关的有7个。华蟾素主要成分与胃癌关键靶点间有较好的结合活性，核心靶点为EGFR、MAPK3、ALB,与胃癌预后密切相关。结论 华蟾素治疗胃癌的关键成分为华蟾毒它灵、蟾毒它灵、华蟾酥毒基、蟾蜍色胺C、蟾毒灵，它们可能通过多靶点、多途径来发挥作用。     

Effects of berberine on colon dermal cell apoptosis in mice with ulcerative colitis based on JAK/STAT signaling pathway北大核心CSCD

Aim To analyze the effects of berberine on the apoptosis of colon epithelial cells and polymorpho-nuclear neutrophils ( PMNs) in mice with ulcerative colitis ( UC ) by regulating JAK/STAT signaling pathway. Methods The UC mouse models were established by dextran sulfate sodium ( DSS) method and were randomly divided into control group, UC group, low-dose, middle-dose and high-dose berberine groups and positive drug group ( mesalazine enteric-coated tablet group) . In addition, the mice were randomly di¬vided into UC group, high-dose berberine group, AG490 group, and high-dose berberine + AG490 group. Levels of serum tumor necrosis factor a (TNF-α) and interleukin 6 (IL-6) and colon epithelial cell apoptosis and PMN apoptosis were compared among the groups. Western blot was used to detect the expres¬sions of colon tissue apoptosis-related and JAK/STAT signaling pathway-related proteins. Results The lev¬els of serum TNF-α and IL-6, apoptosis rate of colon epithelial cell and protein expressions of Fas, FasL, Bax, caspase-3, p-JAK2/JAK2 and p-STAT3/STAT3 in each dose berberine group and positive drug group were significantly lower than those in UC group (P < 0.05), and the above indicators in berberine groups were reduced gradually (P <0.05) . The PMN apoptosis rate and Bcl-2 protein expression were significantly higher in each dose berberine group and positive drug group than those in UC group (P <0. 05) , and the two indicators increased gradually in berberine groups ( P < 0.05). AG490 could reverse the above effects of berberine ( P < 0. 05 ). Conclusions Berberine can inhibit the apoptosis of colon epithelial cell and promote the apoptosis of PMN in UC mice by regulating the JAK/STAT signaling pathway, and then play a role in the treatment of UC. © 2023 Publication Centre of Anhui Medical University. All rights reserved.