| 潘怡宏,王硕,傅华洲.基于JAK/STAT3通路探讨香草扶正合剂治疗非小细胞肺癌机制[J].浙江中西医结合杂志,2025,35(3): |
| 基于JAK/STAT3通路探讨香草扶正合剂治疗非小细胞肺癌机制 |
| Mechanism of Non-small Cell Lung Cancer by Xiangcao Fuzheng Mixture Based on JAK/STAT3 Pathway |
| 投稿时间：2024-06-09 修订日期：2025-02-14 |
| DOI： |
| 中文关键词: 细梗香草 香草扶正合剂 顺铂 肺癌 JAK/STAT3通路 凋亡 |
| 英文关键词:Lysimachia capillipes Hemsl Xiangcao Fuzheng Mixture Cisplatin Lung cancer JAK/STAT3 pathway Apoptosis |
| 基金项目:杭州市卫生科技计划（重点）项目（2018Z02）；国家中医药管理局第七批全国老中医药专家学术经验继承工作室建设项目（No.国中医药人教函〔2022〕76 号）；浙江省名老中医专家传承工作室建设项目（No.GZS2020029） |
|
| 摘要点击次数: 255 |
| 全文下载次数: 1 |
| 中文摘要: |
| 目的 基于Janus激酶(JAK)/信号传导与转录激活因子-3(STAT3)通路探讨香草扶正合剂（XCFZ）治疗非小细胞肺癌的作用及机制。方法 随机抽取8只小鼠作为空白组，其余小鼠建立Lewis肺癌移植瘤模型，随机分为模型组、XCFZ低剂量组、XCFZ中剂量组、XCFZ高剂量组、顺铂组、XCFZ+顺铂组，每组8只。XCFZ低、中、高剂量组分别以XCFZ 9.23、18.46、36.92 g/kg灌胃，每天1次；顺铂组以顺铂3.21 mg/kg腹腔注射，2天1次；XCFZ+顺铂组以顺铂3.21 mg/kg腹腔注射，2天1次，同时XCFZ 18.46 g/kg灌胃，每天1次；空白组和模型组以ddH2O 0.2 mL灌胃，每天1次，连续给药14 d。称取各组小鼠体质量、瘤质量、去瘤后体质量，计算抑瘤率。肿瘤组织石蜡切片行苏木精-伊红(HE)染色和脱氧核糖核酸转移酶介导的缺口末端标记法(TUNEL)染色，观察病理改变。采用蛋白免疫印迹(Western Blot)法检测小鼠肿瘤组织B淋巴细胞瘤-2相关X蛋白( Bax)、B淋巴细胞瘤-2(Bcl-2)、JAK2、磷酸化JAK2(p-JAK2)、STAT3、磷酸化STAT3 Tyr705位点（p-STAT3 Tyr705）、磷酸化STAT3 Ser727位点（p-STAT3 Ser727）蛋白表达水平，实时荧光定量PCR（RT-qPCR）检测肿瘤组织Bax、Bcl-2、JAK2、STAT3 mRNA表达水平。结果 与模型组比较，XCFZ低、中、高剂量组，顺铂组、XCFZ+顺铂组瘤质量[（1.03±0.28）g、（0.73±0.31）g、（1.03±0.13）g、（0.64±0.29）g、（0.62±0.27）g比（1.64±0.26）g，P＜0.05]降低，XCFZ中剂量组去瘤后体质量[（21.25±1.39）g比（19.35±1.81）g，P＜0.05]升高；各给药组小鼠肿瘤组织细胞破坏及凋亡现象明显增多；XCFZ低、中、高剂量组，顺铂组、XCFZ+顺铂组Bax/Bcl-2蛋白比值[（0.25±0.01）、（0.28±0.04）、（0.17±0.01）、（0.26±0.01）、（0.34±0.05）比（0.13±0.02），P＜0.05]及mRNA比值[（4.45±0.19）、（5.64±0.19）、（3.66±0.28）、（5.52±0.79）、（5.58±0.38）比（1.17±0.08），P＜0.05]升高；p-JAK2 / JAK2[（1.23±0.07）、（0.90±0.23）、（1.30±0.09）、（0.69±0.17）、（0.47±0.06）比（1.68±0.06），P＜0.05]、p-STAT3 Tyr705 / STAT3[（9.58±0.75）、（3.97±0.10）、（9.76±0.39）、（3.86±0.04）、（2.70±0.08）比（12.51±0.86），P＜0.05]、p-STAT3 Ser727 / STAT3[（1.93±0.50）、（1.25±0.46）、（2.33±0.71）、（1.32±0.54）、（1.09±0.75）比（3.76±0.54），P＜0.05]蛋白比值，JAK2 [（16.82±1.96）、（13.89±0.39）、（15.54±0.80）、（19.20±0.38）、（18.43±0.85）比（21.41±0.83），P＜0.05]、STAT3[（0.08±0.01）、（0.06±0.00）、（0.09±0.00）、（0.06±0.01）、（0.05±0.03）比（0.10±0.02），P＜0.05]mRNA表达降低。 |
| 英文摘要: |
| Objective To investigate the effect and mechanism of non-small cell lung cancer by Xiangcao Fuzheng Mixture (XCFZ) based on JAK/STAT3 pathway. Methods C57BL/6 mice were randomly selected as blank group (n=8), Lewis lung cancer transplanted tumor model mice were established and randomly divided into six groups (n=8 per group): model group, XCFZ low-dose group, XCFZ medium-dose group, XCFZ high-dose group, cisplatin group, XCFZ and cisplatin group. XCFZ low-dose, medium-dose, and high-dose group were gavaged by XCFZ 9.23, 18.46, and 36.92 g/kg, respectively, once a day. Cisplatin group were intraperitoneally by cisplatin 3.21 mg/kg, once ever 2 days. XCFZ and cisplatin group were gavaged by XCFZ 18.46 g/kg once a day, and intraperitoneally by cisplatin 3.21 mg/kg, once ever 2 days. Blank group and model group were gavaged by ddH2O 0.2mL, once a day. Each group of mice were given drugs for 14 days. The body mass, tumor mass and body mass after tumor removal were weighed, the tumor inhibition rate was calculated. The pathological changes were observed by HE and TUNEL staining in paraffin sections. The protein expression levels of Bax, Bcl-2, JAK2, p-JAK2, STAT3, p-STAT3 Tyr705 and p-STAT3 Ser727 was detected by Western Blot. The mRNA expression levels of Bax, Bcl-2, JAK2 and STAT3 was detected by RT-qPCR. Results Compare with the model group, the XCFZ low-dose, medium-dose, high-dose group, cisplatin group, and XCFZ and cisplatin groups showed significant decrease in tumor mass [(1.03±0.28)g, (0.73±0.31)g, (1.03±0.13)g, (0.64±0.29)g, (0.62±0.27)g vs. (1.64±0.26)g, P＜0.05], XCFZ medium-dose group showed significant increase in the body mass of mice [(21.25±1.39)g vs. (19.35±1.81)g，P＜0.05]. The XCFZ low-dose, medium-dose, high-dose group, cisplatin group, and XCFZ and cisplatin groups also showed significant increase in phenomenon of cell destruction and apoptosis in tumor tissues. Bax/Bcl-2 protein ratios [(0.25±0.01), (0.28±0.04), (0.17±0.01), (0.26±0.01), (0.34±0.05) vs. (0.13±0.02), P＜0.05]，mRNA ratios [(4.45±0.19), (5.64±0.19), (3.66±0.28), (5.52±0.79), (5.58±0.38) vs. (1.17±0.08), P＜0.05] were all significant increased. P-JAK2 / JAK2 protein ratios [(1.23±0.07), (0.90±0.23), (1.30±0.09), (0.69±0.17), (0.47±0.06) vs. (1.68±0.06), P＜0.05], p-STAT3 Tyr705 / STAT3 protein ratios [(9.58±0.75), (3.97±0.10), (9.76±0.39), (3.86±0.04), (2.70±0.08) vs. (12.51±0.86), P＜0.05], p-STAT3 Ser727 / STAT3 protein ratios [(1.93±0.50), (1.25±0.46), (2.33±0.71), (1.32±0.54), (1.09±0.75) vs. (3.76±0.54), P＜0.05]，JAK2 [(16.82±1.96), (13.89±0.39), (15.54±0.80), (19.20±0.38), (18.43±0.85) vs. (21.41±0.83), P＜0.05]、STAT3 [(0.08±0.01), (0.06±0.00), (0.09±0.00), (0.06±0.01), (0.05±0.03) vs. (0.10±0.02), P＜0.05] mRNA were all significant decreased. Conclusion The mechanism of XCFZ in the treatment of non-small cell lung cancer may be related to affecting JAK/STAT3 pathway and inducing cancer cell apoptosis. |
| 查看全文 查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
