Introduction: Type 5 phosphodiesterase inhibitor (PDE5I) that
is well-known effective via NO-cGMP pathway is widely used in
diabetic erectile dysfunction (ED). Whether there is any other
mechanism of PDE5I treatment in diabetic ED that is not clear.
Aim: To clarify the antioxidation role in diabetic ED treatment
by a long-term administration of PDE5I.
Methods: Three groups of Sprague-Dawley rats were utilized:
Group N: Normal control; Group D: Streptozotocin (STZ) induced
diabetic rats as control; Group D+T: STZ induced diabetic rats by
the intragastric administration with tadalafil for eight weeks.
Main outcome measures: Erectile function was assessed by
intracavernous pressure (ICP) and mean arterial pressure (MAP)
during electrical stimulation of cavernous nerve before sacrifice. The
levels of malondialdehyde (MDA), superoxide dismutase (SOD)
and mitochondrial membrane potential (MMP) of cavernous
tissue were assessed by biochemical analysis. The morphology of
mitochondria was observed by electron microscopy.
Results: ICP/MAP ratio was significantly higher in Group D+T
than in Group D. The levels of MDA decreased remarkably and
the activities of SOD increased significantly of Group D+T,
compared with Group D. The level of mitochondrial membrane
potential of cavernous tissue of diabetic rats was partly recovered
by tadalafil treatment for eight weeks. The morphology changes
of mitochondria were also ameliorated in Group D+T.
Conclusions: The long-term administration of tadalafil on diabetic
rats is proven to partly lessen the oxidative stress lesion of the penis
via a local antioxidative stress pathway. Early long-term dosages of
tadalafil once daily maybe partly prevent rats from diabetic erectile
dysfunction. To our knowledge, this is the first report to reveal the
new mechanism on long-term treatment of tadalafil in diabetic ED.