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为了研究大黄素(emodin)对正常的和细菌脂多糖(LPS)刺激的大鼠腹腔巨噬细胞(PM准)释放肿瘤坏死因子琢(TNF-琢)和升高[Ca2+]i的影响,应用L929细胞系和MTT法检测TNF-琢量,同时用激光共焦扫描显微术检测单细胞[Ca2+]i变化动力学。结果显示大黄素能轻度促进正常PM准释放TNF-琢,并发现大黄素诱发PM准[Ca2+]i变化呈振荡波模式。大黄素显著抑制LPS刺激PM准过度释放TNF-琢和升高[Ca2+]i,10-5mol/L大黄素抑制了10mg/LLPS刺激的TNF-琢峰值的50%和[Ca2+]i峰值的68%。LPS诱发PM准[Ca2+]i变化呈现高幅值的“平台期”,大黄素使之转变为低幅值的波动变化。以上结果说明,大黄素对PM准释放TNF-琢和升高[Ca2+]i表现出的双向调节作用之间有一定的相关性,大黄素对LPS诱发的[Ca2+]i升高的调制,可能是抑制LPS刺激PM准释放TNF-琢的信号传导通路中的重要环节。
To investigate the effects of emodin on normal and bacterial lipopolysaccharide (LPS)-stimulated rat peritoneal macrophages (PM)-induced release of tumor necrosis factor 琢 (TNF-琢) and increased [Ca2+]i, L929 cell line and MTT assay were used to detect the amount of TNF-α, and the confocal laser scanning confocal microscopy was used to detect the kinetic change of [Ca2+]i in single cells. The results showed that emodin can slightly promote the release of TNF-琢 from normal PMs, and it was found that emodin-induced PM quasi [Ca2+]i changes to an oscillatory wave pattern. Emodin significantly inhibited the release of TNF-琢 and increased [Ca 2+ ]i by LPS-stimulated PM quasi-immunotherapy, and 10-5 mol/L emodin inhibited 10% of the TNF-琢 peak stimulated by 10 mg/LLPS and [Ca 2+ ]i peak. 68 %. The LPS-induced PM quasi [Ca2+]i changes show a high amplitude of the “platform phase”, emodin makes it into a low amplitude fluctuations. The above results indicate that there is a certain correlation between emodin on the bidirectional regulation of PM release from quasi-release TNF-琢 and [Ca2+]i, and modulation of emodin on LPS-induced [Ca2+]i elevation may be relevant. It is an important part of the signal transduction pathway that inhibits the release of TNF-琢 from PMs stimulated by LPS.