Angiotensin (1-7)

This compound prevents the decrease of the myotube diameter and MHC Levels Induced by myostatin in C₂C₁₂ cells. Angiotensin (1-7) decreases the myostatin-dependent increment of E3 ubiquitin ligases and ROS, the NF-κB signaling induced by myostatin, the myostatin-dependent activity through the mas receptor and Akt/PKB activity in C₂C₁₂ myotubes.[1]

The C₂C₁₂ cells are differentiated until day 5 by changing DMEM–FSB to DMEM supplemented with horse serum. The myotubes are incubated with 1 µg/ml of human recombinant myostatin and/or 10 nM of Angiotensin (1-7). For Akt/PKB inhibition, the myotubes are treated with 10 µM of MK2206, or with 10 µM of A779 antagonist for Mas receptor inhibition. In brief, the procedure is as follows: differentiated cells are pre-treated with this compound for 30 or 60 min, depending on the experiments, and then treated with myostatin.

Daily administration of Angiotensin (1-7) significantly reduces colitis severity observable at both gross and histological levels in DSS treated mice. The anti-inflammatory effects of this compound treatment are associated with a reduction in the phosphorylated forms of p38 MAPK, ERK1/2 and Akt post DSS induction, and its anti-inflammatory properties are in part mediated through reduction of Ang II levels.[3]