Changes of glucocorticoid receptor in hepatic cytoplasm in scalded rats and its regulation by α-MSH and KPV peptide / 第三军医大学学报

Objective　To observe the changes of glucocorticoi d receptor (GR) in hepatic cytoplasm in rats after scalding-induced pathologic al stress and its regulation. Methods　The receptor binding capa city (R0) and the apparent dissociation constant (Kd) of GR in hepatic cytopla sm of normal, low-degree and heavy-degree scalded rats were measured with rad io-ligand binding assay, with ［3H］ dexamethasone as ligand. The changes of R0 and Kd of GR were regulated by injections of anti-rat TNFα, IL-1β a ntibodies, α-melanocyte-stimulating hormone (α-MSH), and KPV peptide( Ac- D-Lys-L-Pro-D-Val) respectively in vivo. Results　The R 0 of GR in hepatic cytoplasm in rats 12 h after heavy-degree scalding ［Mass action robust: （205.52±30.14） fmol/mg; Scatchard: （208.45±30.78） fmol/mg ］were significantly lower than that of control group ［Mass action robust:（307 .86±24.22） fmol/mg;Scatchard:（306.71±27.96） fmol/mg］(P<0.01), but no s ignificant difference was found in the R0 of GR between the control and the ra ts 12 h after low-degree scalding ［Mass action robust: （285.19±16.62） fmol/ mg ; Scatchard: （296.64±16.06） fmol/mg］. The injection of anti-rat TNFα, IL-1β antibodies, α-MSH and KVP all prevented the decline of R0 of GR in h epatic cytoplasm in rats with severe scalding. Conclusion　The injections of anti-rat TNFα, IL-1β antibodies, α-MSH or KPV can attenuate the reduction of GR in rat hepatic cytoplasm caused by severe scalding-induced pathological stress to some extent.

Changes of glucocorticoid receptor in hepatic cytoplasm in scalded rats and its regulation by α-MSH and KPV peptide / 第三军医大学学报

Objective　To observe the changes of glucocorticoi d receptor (GR) in hepatic cytoplasm in rats after scalding-induced pathologic al stress and its regulation. Methods　The receptor binding capa city (R0) and the apparent dissociation constant (Kd) of GR in hepatic cytopla sm of normal, low-degree and heavy-degree scalded rats were measured with rad io-ligand binding assay, with ［3H］ dexamethasone as ligand. The changes of R0 and Kd of GR were regulated by injections of anti-rat TNFα, IL-1β a ntibodies, α-melanocyte-stimulating hormone (α-MSH), and KPV peptide( Ac- D-Lys-L-Pro-D-Val) respectively in vivo. Results　The R 0 of GR in hepatic cytoplasm in rats 12 h after heavy-degree scalding ［Mass action robust: （205.52±30.14） fmol/mg; Scatchard: （208.45±30.78） fmol/mg ］were significantly lower than that of control group ［Mass action robust:（307 .86±24.22） fmol/mg;Scatchard:（306.71±27.96） fmol/mg］(P<0.01), but no s ignificant difference was found in the R0 of GR between the control and the ra ts 12 h after low-degree scalding ［Mass action robust: （285.19±16.62） fmol/ mg ; Scatchard: （296.64±16.06） fmol/mg］. The injection of anti-rat TNFα, IL-1β antibodies, α-MSH and KVP all prevented the decline of R0 of GR in h epatic cytoplasm in rats with severe scalding. Conclusion　The injections of anti-rat TNFα, IL-1β antibodies, α-MSH or KPV can attenuate the reduction of GR in rat hepatic cytoplasm caused by severe scalding-induced pathological stress to some extent.