Deoxyandrographolide (14-deoxyandrographolide) potentiates NGF-induced neurite outgrowth. Deoxyandrographolide suppresses the production of proinflammatory mediators TNF-α and IL-6.

Treatment with 14-deoxyandrographolide (14-DAG) activated AMPK through induction of cyclic AMP-protein kinase A pathway [1]. 14-DAG down-regulated the formation of a death-inducing signaling complex, resulting in the desensitization of hepatocytes to TNF-alpha-induced apoptosis. Pretreatment of hepatocytes with 14-DAG accentuated microsomal Ca-ATPase activity through induction of NO/cGMP pathway [2]. 14-DAG, in concentrations between 10-100 μM, reduced the extracellular acidification rate and the intracellular alkalinization in a dose-dependent manner. In addition, 14-DAG reduced PAF-induced calcium flux in the presence of extracellular calcium, and tyrosine phosphorylation of a 44 kDa protein corresponding to the MAPK(ERK1) [3].

The protective effect of 14-DAG against ethanol-induced hepatic injury is based on its ability to reduce oxidative stress through cNOS dependent improvement of redox status. 14-DAG mediated activation of adenylate cyclase-cAMP signaling leading to the up-regulation of cNOS may provide a promising approach in the prevention of liver diseases during chronic alcoholism [4].