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目的研究九龙藤总黄酮对缺氧/复氧乳鼠心肌细胞的影响及作用机制。方法建立心肌细胞缺氧/复氧损伤模型,给予不同剂量九龙藤总黄酮(终质量浓度分别50、100、200 mg·L-1)预处理,倒置显微镜下观察心肌细胞形态学变化;酶联免疫法测定肿瘤坏死因子活性;免疫组化方法观察Bcl-2、Bax、NF-κB蛋白的表达;Annex v-FITC/PI双染法测定心肌细胞凋亡率。结果与模型组相比,九龙藤总黄酮预处理能减轻心肌细胞损伤,降低肿瘤坏死因子-α、诱导型一氧化氮合酶、维持内皮型一氧化氮合酶水平,上调Bcl-2、下调Bax、NF-κβ蛋白表达,抑制心肌细胞凋亡(P<0.01或P<0.05)。结论九龙藤总黄酮对缺氧/复氧心肌损伤具有保护作用,其机制可能与调节诱导型一氧化氮合酶、核转录因子-κβ信号通路,上调Bcl-2、下调Bax和核转录因子-κB蛋白表达,抑制心肌细胞凋亡有关。
Objective To study the effects of total flavonoids from Jiulongtang on cardiomyocytes in hypoxia / reoxygenation rats and its mechanism. Methods Hypoxia / reoxygenation injury model was established in rats. Cardiomyocytes were pretreated with different doses of total flavonoids (50, 100, 200 mg · L-1, respectively), and morphological changes of myocardial cells were observed under inverted microscope. The activity of tumor necrosis factor (TNF) was measured by immunohistochemistry. The expressions of Bcl-2, Bax and NF-κB were detected by immunohistochemistry. The apoptosis rate of cardiomyocytes was detected by Annex V-FITC / PI double staining. Results Compared with the model group, pretreatment with total flavonoids of Jiulongtang could reduce the injury of cardiomyocytes, decrease the levels of tumor necrosis factor-α and inducible nitric oxide synthase, maintain the level of endothelial nitric oxide synthase, upregulate Bcl-2 Bax, NF-κβprotein expression, inhibit cardiomyocyte apoptosis (P <0.01 or P <0.05). Conclusions Total flavonoids from Radix Jiulong can protect against hypoxia / reoxygenation myocardial injury. The mechanism may be related to the regulation of inducible nitric oxide synthase, nuclear factor-κβ signaling pathway, up-regulation of Bcl-2, down-regulation of Bax and nuclear transcription factor- κB protein expression, inhibition of myocardial cell apoptosis related.