Toxicological mechanisms of compatibility application of Sargassum pallidum-Glycyrrhiza uralensis on kidney in rats / 中草药

ABSTRACT

Objective To study the toxicological mechanisms of the compatibility application of Sargassum pallidum and Glycyrrhiza uralensis on kidney in rats. Methods Rats were divided into control, Sargassum pallidum (S), Glycyrrhiza uralensis (G), and Sargassum pallidum-Glycyrrhiza uralensis extract (S-G) groups, which were respectively exposed (gavages) for 4 weeks. Then, the levels of blood urea nitrogen (BUN), serum creatinine (Scr), aldosterone, cortisol, and electrolytes in rat serum and pathological sections of kidney were detected. Six active contents of Glycyrrhiza uralensis in kidney of rats were detected by UPLC-TQ/MS method. The expression of HSD11B2 in kidney was detected by Western blotting. Results Compared with the control group, all biochemical indicators of S group had no obvious change. It was found that the level of aldosterone from G group and S-G group was significantly lower than that from control group (P < 0.05, 0.01). In contrast to the control group, S. pallidum-G. uralensis extract led to significantly increased concentration of cortisol, BUN, and Scr in serum (P < 0.05, 0.01). The level of K+ and Cl- in S-G group was significantly lower than that in control group (P < 0.05, 0.01). Pathological examination showed that the G group had mild inflammation infiltration, and a serious inflammatory response accompanied by protein tube was absolved in S-G group. Compared with the G. uralensis extract group, the combination of S. pallidum and G. uralensis significantly raised the concentration of glycyrrhetinic acid (GA) in kidney (P < 0.05).When compared to that of control group, there was an inhibited expression of HSD11B2 in the kidney of L group and S-G group. Moreover, the expression of HSD11B2 in S-G group was markedly higher than that in G group (P < 0.05). Conclusion The toxicity of S-G group was mainly result that increased accumulation of GA, and inhibited the expression of HSD11B2, which resulted the aldosterone-cortisol system disorders.