Higuchi H, Katoh N, Miyamoto T, Uchida E, Yuasa A, Takahashi K
Department of Veterinary Biochemistry, Rakuno Gakuen University, Ebetsu, Japan.
Am J Vet Res. 1994 Aug;55(8):1080-5.
Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10(-12) to 10(-4) M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10(-8) to 10(-6) M dexamethasone. Haptoglobin release was similarly induced by cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10(-8) M dexamethasone. Dexamethasone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.
从雄性小牛的肝脏中分离出实质细胞，对形成的单层培养物用糖皮质激素进行处理，以检查触珠蛋白是否由类固醇激素诱导产生，触珠蛋白的出现与牛的肝脂肪变性（脂肪肝）有关。在不添加地塞米松的情况下，培养基中仅检测到微量的触珠蛋白。添加地塞米松（10^(-12)至10^(-4)M）后，大量的触珠蛋白释放到培养基中。在地塞米松浓度为10^(-8)至10^(-6)M时观察到最大释放量。皮质醇同样能诱导触珠蛋白释放，尽管其作用不如地塞米松强。放线菌素D（一种已知的蛋白质合成抑制剂）能剂量依赖性地减少对10^(-8)M地塞米松反应而释放的触珠蛋白量。地塞米松还能诱导膜联蛋白I的产生，已知膜联蛋白I是对糖皮质激素作出反应而合成的。地塞米松处理导致细胞胞质溶胶中的蛋白激酶C活性降低，这已被证明是地塞米松处理细胞中的早期事件。除糖皮质激素外，雌二醇能诱导触珠蛋白释放，而孕酮的作用较小。触珠蛋白与肝脂肪变性的关联可以通过以下事实得到合理的解释：肝脏中触珠蛋白的产生是由糖皮质激素和雌二醇诱导的，而这些类固醇激素是牛肝脂肪变性发展的触发因素。
