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        雙氫青蒿素對低氧下人肺動脈內(nèi)皮細胞增殖和分泌功能影響

        2020-04-05 18:50:20余華王良興劉靜靜董一枝夏曉茹管華琴
        中國現(xiàn)代醫(yī)生 2020年4期

        余華 王良興 劉靜靜 董一枝 夏曉茹 管華琴

        [摘要] 目的 探討雙氫青蒿素(Dihydroartemisinin,DHA)對低氧條件下人肺動脈內(nèi)皮細胞的數(shù)量和功能影響,尋找治療低氧性肺動脈高壓的新方法。 方法 將人肺動脈內(nèi)皮細胞株進行復(fù)蘇、傳代、鑒定,然后細胞實驗分為常氧組、低氧組、低氧+DHA干預(yù)組,造模48 h后,分別檢測人肺動脈內(nèi)皮細胞的增殖能力(CCK-8法)、ELISA法檢測細胞上清液中超氧物歧化酶(SOD)活性和一氧化氮(NO)含量。 結(jié)果 常氧組、低氧組、低氧+DHA干預(yù)組的CCK-8法檢測OD值分別為(0.813±0.012)、(0.905±0.018)、(0.842±0.015),各組間比較差異有統(tǒng)計學(xué)意義(P<0.05);各組SOD活力檢測分別為(40.665±0.865)U/mL、(12.988±0.556)U/mL、(26.376±0.831)U/mL, 各組間比較差異有統(tǒng)計學(xué)意義(P<0.05);各組 NO含量分別為(23.803±0.778)μmol/L、(48.668±0.881)μmol/L、(37.497±0.793)μmol/L,各組間比較差異有統(tǒng)計學(xué)意義(P<0.05)。 結(jié)論 DHA可以抑制低氧誘導(dǎo)下人肺動脈內(nèi)皮細胞的增殖能力,改善低氧誘導(dǎo)下SOD活性和抑制低氧誘導(dǎo)下分泌NO的能力;提示DHA對低氧誘導(dǎo)的人肺動脈內(nèi)皮細胞具有保護作用,推測其對低氧性肺動脈高壓的形成可能具有拮抗作用。

        [關(guān)鍵詞] 雙氫青蒿素;低氧;肺動脈內(nèi)皮細胞;肺動脈高壓

        [中圖分類號] R563.9? ? ? ? ? [文獻標(biāo)識碼] A? ? ? ? ? [文章編號] 1673-9701(2020)04-0015-04

        Effects of dihydroartemisinin on proliferation and secretion of human pulmonary artery endothelial cells under hypoxia

        YU Hua1? ?WANG Liangxing2? ?LIU Jingjing2? ?DONG Yizhi2? ?XIA Xiaoru3? ?GUAN Huaqin2

        1.Department of Cadre Health, the First Affiliated Hospital of Wenzhou Medical University, Hangzhou? ?325000,China;2.Department of Respiratory Medicine, the First Affiliated Hospital of Wenzhou Medical University, Hangzhou? ?325000,China;3.Department of Rheumatology and Immunology, the First Affiliated Hospital of Wenzhou Medical University, Hangzhou? ?325000,China

        [Abstract] Objective To investigate the effects of dihydroartemisinin (DHA) on the number and function of human pulmonary artery endothelial cells under hypoxic conditions, and to find a new treatment for hypoxic pulmonary hypertension. Methods Human pulmonary artery endothelial cells were resuscitated, passaged and identified. Then the cells were divided into normoxia group, hypoxia group and hypoxia+DHA group. Human pulmonary artery endothelial cells were resuscitated, passaged and identified. Then the cells were divided into normoxia group, hypoxia group and hypoxia+DHA group. After 48 hours of modeling, the proliferation of human pulmonary artery endothelial cells was detected (CCK8 method). The superoxide dismutase (SOD) activity and nitric oxide (NO) content in the cell supernatant were determined by ELISA method. Results The OD values of CCK-8 method in normoxia group, hypoxia group and hypoxia+DHA group were (0.813±0.012), (0.905±0.018), and (0.842±0.015), respectively. The differences between the groups were statistically significant (P<0.05). The SOD activity of each group was (40.665±0.865)U/mL, (12.988±0.556)U/mL, and (26.376±0.831)U/mL, and the differences were statistically significant (P<0.05). The NO content of each group were (23.803±0.778)μmol/L, (48.668±0.881)μmol/L, and (37.497±0.793)μmol/L, and the differences were statistically significant among groups. Conclusion DHA can inhibit the proliferation of human pulmonary artery endothelial cells induced by hypoxia, improve the activity of SOD and inhibit the secretion of NO; suggesting that DHA has protective effect on hypoxia-induced human pulmonary artery endothelial cells, and it may have an antagonistic effect on the formation of hypoxic pulmonary hypertension.

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