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目的：观察β阻滞剂及其对映异构体对ＴＮＦα诱发的心肌细胞信号转导异常的拮抗作用。方法：用体外培养的乳鼠心肌细胞进行β受体密度、Ｇ蛋白、ＡＣ活性及ＰＫＡ活性测定。结果：ＴＮＦα下调β受体密度；下调Ｇｓ蛋白，上调Ｇｉ蛋白，降低Ｇｓ／Ｇｉ比值；细胞内ｃＡＭＰ水平升高；激活ＰＫＡ，总ＰＫＡ水平升高。此作用能被β阻滞剂的Ｒ（＋）型对映体而不是Ｓ（－）型对映体所拮抗。结论：β阻滞剂的Ｒ（＋）型对映体有较好的拮抗ＴＮＦα介导的细胞毒作用，可能有利于对心衰的治疗。
OBJECTIVE: To observe the antagonism of β-blockers and their enantiomers on TNFα-induced cardiomyocyte signal transduction abnormalities. Methods: The β - cell density, G protein, AC activity and PKA activity of neonatal rat cardiomyocytes were measured. Results: TNFα downregulated β receptor density; down-regulated Gs protein, up-regulated Gi protein, decreased Gs / Gi ratio; increased intracellular cAMP level; activated PKA, total PKA level increased. This effect can be antagonized by the R (+) enantiomer rather than the S (-) enantiomer of the beta blocker. CONCLUSION: The R (+) enantiomer of β-blocker antagonizes TNFα-mediated cytotoxicity and may be beneficial to the treatment of heart failure.