The immunohistochemical study of specimens was performed with monoclonal HHF35 and polyclonal C4d in an attempt to establish the mechanism of action of the drugs, given that the former is a marker for muscle cells and the C4d is a marker for the inflammatory process mediated by the complement system. Ylä-Herttuala et al. demonstrated the action of the complement system in atherosclerotic lesions and Tsai et al. identified the inhibitory activity of p38 by using cilostazol. Since the inhibition of p38 has been associated with possible therapeutic effects on autoimmune diseases and inflammatory processes, we chose to assess the effect of A. sativum on inflammation through the complement system; then we used the marker C4d. However, in all animals, no statistical difference was observed with regard to muscle invasion in the intima as well as the inflammatory process mediated by the complement system in the myointimal wall. Therefore, the study was not able to characterize the manner in which the inhibition or decrease of myointimal hyperplasia occurred, given that there was no statistically significant inhibition of muscle invasion or reduction of the inflammatory process, with the use of A. sativum or cilostazol.