Cordycepin modulates body weight by reducing prolactin via an adenosine A1 receptor.

In this study, we explored the molecular mechanism of the anti-obesity effect of cordycepin. In vivo, obese rats model was induced by high fat diet for 5 weeks, the serum and liver lipids coupled with serum prolactin were reduced by treatment of cordycepin (P<0.01) , the results suggested that cordycepin is a potential drug for lowering blood and liver lipids and reducing body weight which related with prolactin. Cordycepin also protects adipocytes from enlargement and hepatocytes from lipotoxicity caused inflammation. In vitro, cordycepin could inhibit prolactin secretion in GH3 cells via upregulating the expression of adenosine A1 receptor, the inhibition effect could be blocked by an antagonist of adenosine receptor A1 DPDPX, which demonstrated that cordycepin may work as an adenosine agonist. In addition, cordycepin could inhibit ERK/AKT/PI3K pathway in GH3 cells. Meanwhile, cordycepin could block prolactin induced the upregulation of lipogenesis genes PRLR, and phosphorylation of JAK2 in 3T3-L1 cells. In vivo study, cordycepin would down-regulate the expression of prolactin receptor (PRLR) but not phosphorylation of JAK2. Thus, we concluded that cordycepin modulate body weight by reducing prolactin release via an adenosine A1 receptor. PMID: 30124145 [PubMed - as supplied by publisher]
Source: Current Pharmaceutical Design - Category: Drugs & Pharmacology Authors: Tags: Curr Pharm Des Source Type: research