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在培养心肌细胞缺氧－再给氧模型上，发现牛磺酸（２０ｍｍｏｌ·Ｌ－１，终浓度）能显著降低细胞内脂质过氧化物（ＬＰＯ）荧光强度；剂量依赖性地提高心肌细胞超氧化物歧化酶（ＳＯＤ）活性；以荧光比率法（荧光探针为Ｉｎｄｏ－１－ＡＭ）在粘附式细胞仪（ＡＣＡＳ５７０）上测定细胞内游离Ｃａ２＋荧光比率，结果显示缺氧及再给氧后细胞内Ｃａ２＋荧光比率明显升高，２０ｍｍｏｌ·Ｌ－１牛磺酸能显著减少Ｃａ２＋荧光比率；分别以２０ｍｍｏｌ·Ｌ－１、０．４ｍｍｏｌ·Ｌ－１Ｃａ２＋及０．１ｍｍｏｌ·Ｌ－１维拉帕米处理细胞，牛磺酸能降低高Ｃａ２＋引起的细胞搏动加快；而提高低Ｃａ２＋及维拉帕米处理后的细胞搏动。提示牛磺酸对培养心肌细胞再给氧损伤有保护作用，其机理与其提高心肌细胞ＳＯＤ活性、降低细胞内游离Ｃａ２＋浓度及对细胞Ｃａ２＋双向调节作用有关。
In cultured cardiomyocytes hypoxia-reoxygenation model, taurine (20mmol·L-1, final concentration) was found to significantly reduce the intracellular lipid peroxide (LPO) fluorescence intensity; a dose-dependent increase in myocardial cells Superoxide dismutase (SOD) activity. Intracellular free Ca2 + fluorescence was detected by fluorescence ratio method (fluorescent probe Indo-1-AM) on adherent cytometer (ACAS570) The intracellular Ca2 + fluorescence ratio was significantly increased after oxygen treatment, and 20mmol·L-1 taurine significantly reduced the Ca2 + fluorescence ratio. The ratio of Ca2 + fluorescence was significantly decreased in 20mmol·L-1, 0.4mmol·L-1Ca2 + and 0.1mmol·L- When treated with lapatimine, taurine decreased the cell cycle velocity induced by high Ca2 + concentration and increased the cell beating rate after low Ca2 + and verapamil treatment. These results suggest that taurine can protect cultured cardiomyocytes from reoxygenation injury and its mechanism is related to the increase of SOD activity in cardiomyocytes, decrease of intracellular free Ca2 + concentration and the bidirectional regulation of Ca2 + in cells.