丹参制剂治疗急性胰腺炎的机制研究

急性胰腺炎(AP)是临床常见的急腹症,由于病情重,并发症多,导致病死率较高,发病机制复杂,到目前为止仍不能明确。中、西医方法具有各自特色,其中丹参作为常见药物之一,因具有活血化瘀、消肿止痛的功效,广泛地用于治疗AP,其中以水溶性成分入药的丹参制剂为主,临床应用中西医治疗方案联合丹参制剂较单纯使用西医方法治疗AP疗效显著。     

高良姜素通过PI3K/Akt及p38-MAPK信号通路增强胃癌SGC-7901细胞对阿帕替尼的敏感性

摘要：目的 探讨高良姜素对阿帕替尼抗胃癌作用的影响及可能机制。方法 体外培养胃癌SGC-7901细胞, 3-（4,5-二甲基噻唑-2）-2,5-二苯基四氮唑溴盐（MTT）法筛选出高良姜素和阿帕替尼抑制胃癌细胞增殖的合适浓 度。将胃癌细胞分为4组：空白对照组、高良姜素组、阿帕替尼组和高良姜素+阿帕替尼组。MTT法检测细胞增殖活 力;流式细胞术检测细胞凋亡率;细胞划痕实验和Transwell小室实验分别检测细胞迁移和侵袭能力;Western blot检 测细胞凋亡及PI3K/Akt及p38-MAPK信号通路相关蛋白表达。结果 阿帕替尼和高良姜素均显著抑制胃癌SGC- 7901细胞的增殖,并呈浓度依赖性（P＜0.05）,20 mg/L阿帕替尼和300 mg/L高良姜素是最佳的干预浓度。与20 mg/L 阿帕替尼组相比,高良姜素+阿帕替尼组可以明显抑制胃癌SGC-7901细胞的增殖、迁移和侵袭（P＜0.05）。流式细 胞术结果显示,高良姜素+阿帕替尼组对胃癌SGC-7901细胞促凋亡作用明显优于20 mg/L阿帕替尼组（P＜0.05）。 Western blot结果显示,高良姜素+阿帕替尼组Bcl-2相关X蛋白（Bax）、磷酸化蛋白激酶B（p-Akt）、磷酸化丝裂原活 化蛋白激酶（p-p38）蛋白表达明显高于20 mg/L阿帕替尼组,B淋巴细胞瘤-2（Bcl-2）蛋白明显低于20 mg/L阿帕替尼 组（P＜0.05）。结论 高良姜素可能通过抑制PI3K/Akt和激活p38-MAPK信号通路增强阿帕替尼抗胃癌SGC-7901 细胞的作用。     

Effect of galangin on hypoxia-inducible factor-1α-mediated epithelial mesenchymal transformation in gastric cancer cells北大核心CSCD

Aim To investigate the effect of galangin(GLA) on gastric cancer in hypoxic microenvironment. Methods The gastric cancer SGC-7901 cell line was induced with CoCl2 to mimic the hypoxic tumor microenvironment in vitro. Cell viability assay was performed using CCK- 8 reagents. Invasive Ability of Cancer Cells was Analyzed by Transwell Assay. And the expression levels of relevant genes we detecting and rt-QPcr. Results the study showed that low, Medium and High Concentrations of GLA (50, 100 and 150 μmol ·L-1)presented a dose-dependent inhibition of CoCl2 -induced gastric cancer SGC-7901 cell viability. This concentration gradient also showed significant inhibition on cell invasion after CoCl2 intervention(P<0.01). In-depth study revealed that the CoCl2 -induced increased HIF-1α protein expression was inhibited with increasing GLA concentration, while HIF-1α mRNA expression was not affected. Meanwhile, Snail and Vimentin expression of epithelial mesenchy bad transition-related genes significantly increased with increasing GLA dose(P<0.05), whereas E-cadherin expression significantly decreased(P<0.01). Conclusions GLA inhibits HIF-1α expression and epithelial mesenchymal transition under tumor hypoxia, thereby s uppressing gastric cancer development. © 2023 Publication Centre of Anhui Medical University. All rights reserved.