知母皂甙元对家兔氢化可的松模型血淋巴细胞β受体的作用

The effect of sarsasapogenine on peripheral lymphocyle β-adrenoceptors in rabbit hydrocortison models

用放射性配基结合分析法和放射免疫分析法测定了家兔肌注氢化可的松(HC)前后血淋巴细胞β-肾上腺素受体(β-AR)和血浆皮质醇(Cor)的变化以及灌服知母皂甙元(SAR)后对它们的影响。结果表明:肌注HC 4d后,家兔血淋巴细胞β-AR的特异结合(SB)由0.65±0.03升至1.48±0.13fmol/10~6细胞(P<0.001);血浆Cor由128.0±20.6升至238.7±45.2nmol/l(P<0.001)。HC连用4d后加用SAR6d,血淋巴细胞β-AR的SB降至0.76±0.06fmol/10~6细胞,与用SAR前相比有显著性差异(P<0.001);血浆Cor为236.9±40.2nmol/L,与用SAR前相比无显著性差异(P>0.05)。本文结果提示:SAR可使家兔肾上腺皮质机能亢进模型(氢可模型)升高了的β-AR数目趋于正常;SAR的这种调整作用与体内Cor水平无关。

The effects of sarsasapogenine (SAR), an active principle of Anemorrhenae Rhizome (知母)on peripheral lymphocyte β-adrenoceptors (β-AR) and serum cortisol contents were studied in rabbit hydrocortison models produced by repeated injections of therapeutic doses of hydrocortisone. The lymphocyte β3-AR binding sites (SB) were measured with 125I-PIN binding assay and the serum cortisol contents were estimated with radioimmunoassay. Experimental data revealed that hydrocortisone treatment markedly elevated the lymphocyte SB (0.65±0.03 and 1.48±0.13 fmol/106 cells before and after treatment) as well as the serum cortisol (128±21 and 239±45 nmol/1 before and after treatment). Oral administration of SAR for 6 days decreased the lymphocyte β-AR significantly (1.48±0.13 and 0.76±0.06 fmol/106 cells before and after administration). On the contrary, SAR showed no significant effect on serum cortisol contents.. Therefore the down-regulation effect of SAR on peripherel lymphocyte β-AR, which might reflect one of the clinical effects of Anemorrhenae Rhizome for treating 'Yin Deficiency'syndrome, is unlikely to be mediated through an influence on serum cortisol content.The mechanism of the down-regulation effect of SAR on peripheral lymphocyte β-AR remains to be studied.