Healing effect of topical nifedipine on skin wounds of diabetic rats

Non-healing foot ulcers in patients with diabetes are the leading causes of complications such as infection and amputation. Ulceration is the most common single precursor to amputation and has been identified as a causative factor in 85% of lower extremity amputations. It seems that poor outcomes are generally associated with infection, peripheral vascular disease and wounds of increasing depth. Nifedipine, a calcium channel blocker that is mainly used for the treatment of cardiovascular disorders has recently been used to treat wounds caused by peripheral vascular disorders. In present study topical Nifedipine 3% has been used to treat skin wounds in normal and diabetic rats. Effects of Nifedipine were evaluated in three different phases of wound healing process. In both experiments [normal and diabetic rats] topical Nifedipine significantly improved inflammatory phase. However, maturation phase was only significantly improved in diabetic rats. Nifedipine did not affect proliferation phase in either group significantly. Overall results of this study showed topical Nifedipine improved skin wound healing process in normal and diabetic rats

Modulation of Mitochondrial Uptake of Adenosine by Nitrobenzylthionosine

In this study the uptake and metabolism of adenosine by mitochondria has been investigated. Incubation of CEM cells mitochondria preparation with [3H]-adenosine showed substantial uptake and metabolism of adenosine. Adenosine was both anabolized to AMP, ADP and ATP, and also catabolized to inosine. The highest concentration of metabolites in extracted mitochondria was due to AMP. The mitochondria preparation did not show any 5'-nucleotidase activity and this will exclude any possibility of the production of adenosine from AMP in the preparation. Coincubation of [3H]-adenosine with mitochondria in the presence of 2 [micro] M of a known potent nucleoside transporter inhibitor, nitrobenzylthioinosine [NBMPR], substantially reduced the mitochondria content of adenosine and its metabolites. The results of this study showed that adenosine was uptaken by the mitochondria preparation. Metabolism of adenosine after incubation with CEM mitochondria provided further evidence for mitochondrial uptake and metabolism of this nucleoside