The glucocorticoid receptor of hepatic cytosol of rat was determined by the exchange assay in the presence of endogenous corticosterone. The condition of ex-chame was 0℃ , 4.5~5 hours. The dissociation of corticosterone-receptor complex was about 90% under such a condition. The effect of the endogenous corticosterore on the assay was evaluated by the measurement of [3H]-dexamethasone binding after preincubation of the liver cytosol from adrenalectomized rats with different amounts of corticosterone. The results indicated that, at a corticosterone concentration of less than 6 nM the error of the specific binding capacity (Ro) of [3H]-dexa-methasone was no more than 10%,and the apparant dissociation constant (Kd) was essentially unchanged. The Ro and Kd of glucocorticoid receptor of the hepatic cytosol of normal and scalded rats were measured by this method. The Ro was decressed in the scalded rats. The levels of Ro in hepatic cytosol from rats after 1, 12,24, 36 hours and 5 days of scalding were 76.4?15.2%,70.6?22.0%79.7?5.8%, 113.0?24.8% and 102.9 ?17.6% (mean?SD) of the control group respectively. The apparant Kd slightly increased 1 hour after scalding. The possible mechanisms of the above changes were discussed.

The high-affinity glucocorticoid binding sites (HAGS) and the low-affinity glucocorticoid binding sites (LAGS) with steroid specificity were demostrated in cerebral cytosol of rats by using the radioligand binding assay. The Kd of HAGS and LAGS were (178?0.71)?l0-8mol/L and (2.12?1.06)?10-6mol/L respecitively as estimated by Scatchard and Pseudoscatchard analysis. Glucocorticoid receptors (GR) in the traumatized(left) hemisphere cytosol were decreased more significantly than those in both the control (right) hemisphere cytosol at 6h postinjury and normal brain tissue (P

Laminin(LN) and hyaluronie acid (HA) are extracellular matrix in liver. The effects of LN and HA on human fetal liver cells proliferation and collagen synthesis were observed and serum levels of LN and HA were assayed m patients with liver diseases by an enzyme immunoassay method. Both LN and HA had a significant effect on the inhibition of cell proliferation and collagen production. However, serum levels of LN and HA were significantly increased in liver cirrhosis comparing with healthy controls and with patients with non-liver diseases. The results suggest that LN and HA may play a role in the feed-back inhibition mechanism in liver fibrogencsis, and assay of LN and HA in serum may be useful to the diagnosis of liver fibrosis.