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目的研究氨基胍对高果糖诱导的大鼠脑基底动脉血管平滑肌细胞增殖的影响和机制。方法原代培养大鼠脑基底动脉血管平滑肌细胞,用CCK8法测定不同浓度(50、100μmo/lL)氨基胍对15和30 mmo/lL果糖预诱导的血管平滑肌细胞增殖的影响。western blotting方法检测高果糖刺激后AKT以及JNK激酶表达的变化;以及检测不同浓度氨基胍预处理后对上述指标的影响。结果高果糖(30 mmo/lL)显著促进大鼠脑基底动脉血管平滑肌细胞增殖(0.768±0.032比0.374±0.054,P<0.01),在给予不同浓度(50、100μmo/lL)氨基胍后,平滑肌细胞增殖明显下降(0.584±0.063和0.387±0.031比0.768±0.032,P<0.01)。高果糖还明显刺激AKT以及JNK蛋白的表达,而给予氨基胍后可有效抑制上述蛋白表达。结论高果糖可诱导脑基底动脉血管平滑肌细胞增殖,而氨基胍可能通过抑制MAPK以及PI3K信号途径改善高果糖对平滑肌的增殖作用。
Objective To investigate the effect and mechanism of aminoguanidine on the proliferation of rat basilar artery smooth muscle cells induced by high fructose. Methods The basilar artery smooth muscle cells of rats were cultured in primary culture. The effects of different concentrations of aminoguanidine (50,100 μmol / L) on the proliferation of vascular smooth muscle cells pre-induced by 15 and 30 mmol / L L-fructose were determined by CCK8 assay. Western blotting was used to detect the changes of AKT and JNK kinase expression after high fructose stimulation; and the effects of different concentrations of aminoguanidine on the above indexes were detected. Results High fructose (30 mmo / L) significantly promoted the proliferation of rat basilar artery smooth muscle cells (0.768 ± 0.032 vs 0.374 ± 0.054, P <0.01). After administration of aminoguanidine at different concentrations (50 and 100 μmol / L) Cell proliferation was significantly decreased (0.584 ± 0.063 and 0.387 ± 0.031 vs 0.768 ± 0.032, P <0.01). High fructose also significantly stimulated AKT and JNK protein expression, and given aminoguanidine can effectively inhibit the above protein expression. Conclusion High fructose can induce the proliferation of vascular smooth muscle cells in basilar artery, while aminoguanidine can improve the proliferation of smooth muscle by high fructose by inhibiting MAPK and PI3K signaling pathway.