Taken all our data together, the present work showed at the very
first time that AL was effective in protecting against myocardial
apoptosis and fibrosis in STZ-induced diabetic rats. Furthermore,
AL treatment is also associated with a dose-dependent increase in
expression of the anti-apoptotic protein Bcl-2, and a decrease inthe pro-apoptotic protein Fas, and similarly, an increase in expressions
of CTGF and TGF-1 proteins. Overall, our data suggested
the potential clinical efficacy of AL in preventing myocardial apoptosis
and fibrosis in diabetes. It is tempting for the application of
AL to be a useful therapeutic management in diabetes with cardiac
injury.