| 杨盼,成林杰,单玮碧,等.间歇性缺氧通过上调蛋白激酶B /哺乳动物雷帕霉素靶蛋白通路促进 S180实体瘤的生长[J].安徽医药,2021,25(4):678-681. |
| 间歇性缺氧通过上调蛋白激酶B /哺乳动物雷帕霉素靶蛋白通路促进 S180实体瘤的生长 |
| Intermittent hypoxia promotes S180 solid tumor growth by upregulating the Akt/mTOR pathway |
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| DOI：10.3969/j.issn.1009-6469.2021.04.010 |
| 中文关键词: 低氧 间歇性缺氧(IH) 肿瘤 蛋白激酶B /哺乳动物雷帕霉素靶蛋白信号通路(Akt/mTOR) 凋亡 蛋白质印迹法(Western blotting) 小鼠 |
| 英文关键词: Hypoxia Intermittent hypoxia (IH) Tumor Threonine kinase/mammalian target of rapamycin (Akt/mTOR signaling pathway) Apoptosis Western blotting Mice |
| 基金项目:国家自然科学基金项目(81860022，81560020) |
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| 中文摘要: |
| 目的探讨间歇性缺氧(Intermittent hypoxia，IH)对 S180实体瘤生长的影响及其可能机制。方法 2018年 3—5月，在新疆医科大学动物房购买的 8周龄清洁级昆明鼠为研究对象，将 16只接种 S180实体瘤的小鼠采用随机数字表法分成 2组:常氧组(Room air，RA)和 IH组，每组 8只， IH暴露两周后处死小鼠，取肿瘤组织称重量， TUNEL法检测肿瘤凋亡情况，蛋白质印迹法(Western blotting)检测丝氨酸 /苏氨酸蛋白激酶(serine/threonine kinase，Akt)、 p-Akt、哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin，mTOR)及 p-mTOR在 RA组和 IH组肿瘤组织中的蛋白表达情况。结果 IH组肿瘤组织重量明显高于 RA组(P<0.05)IH组肿瘤组织凋亡小体数为(81.18±8.92)个，低于 RA组肿瘤组织凋亡小体数(129.75±20.20 P<0.05)IH组肿瘤组织中 Akt、m，TOR的蛋白表达与 RA组差异无统计学意义， IH组肿瘤组织中 p-Akt、p-mTOR的蛋白表达水平明显，增加(P<0.05)。结论 IH可促进小鼠 S180实体瘤的生长，其机制可能同上调 Akt/mTOR通路促进 S180实体瘤的生长并抑制肿瘤组织的凋亡有关。本研究将为睡眠呼吸暂停综合征(Obstructive sleep apnea，OSA)合并肿瘤的治疗提供新的思路。 |
| 英文摘要: |
| Objective To investigate the effects of intermittent hypoxia (IH) on the growth of S180 solid tumor and its possible mechanism.Methods Eight-week-old clean-grade Kunming mice purchased in the Animal Room of Xinjiang Medical University FromMarch to May 2018 were selected as the research objects. Sixteen mice inoculated with S180 solid tumor were randomly assigned into 2groups using a random number table: Room air (RA) group and IH group, 8 mice in each group. The mice were sacrificed after twoweeks of IH exposure, tumor tissues were weighed, and the tumor apoptosis was detected by TUNEL staining, and the expressions ofserine/threonine kinase (Akt), p-Akt, mammalian target of rapamycin (mTOR) and p-mTOR in tumor tissues of RA group and IH group were detected by Western blotting.Results The tumor weights of IH group were significantly heavier than those of RA group (P<0.05).The number of apoptotic bodies in tumor tissues of IH group was (81.18±8.92), which was lower than that in RA group [(129.75 ±20.20), P<0.05). The protein expressions of Akt and mTOR in tumor tissues of IH group were not significantly different from those ofRA group. The protein expression levels of p-Akt and p-mTOR in tumor tissues of IH group increased significantly (P<0.05) compared with RA group.Conclusion IH promotes the growth of S180 solid tumors in mice. The mechanism may be related to the up-regulationof Akt/mTOR pathway and the inhibition of the apoptosis of tumor tissues. This study will provide new ideas for the treatment of tumorscombined with obstructive sleep apnea. |
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