| Summary: | Background: Several genes which their products are involved in the mechanism
of ovulation are induced by the LH surge. One of them is COX-2, which one of
molecular marker in mammals ovulation cycle. LH acts through protein kinase A
(PKA) pathway in granulosa cells. PGV-0 has farmacologic action by inhibiting
prostaglandin biosynthesis in cyclooxygenase pathway. PGV-0 had action simillar
with indometacin (selective COX-2 inhibitor) which cause follicle rupture in
basolateral.
Objectives: The objectives of this study is to investigate inhibition of PGV-0 to
the expression of COX-2 in granulosa cells and to determine the action site of
PGV-0 on COX-2 expression signal transduction in cAMP pathway.
Methods: The subjects in this study were 27 female Rattus norvegicus strain
Sprague Dawley. At the age of 28 days, subjects were induced by 5 IU PMSG.
Rats were stimulated by LH 5 IU, then administered by theophylline 25 mg/kgBW
orally, and PGV-0 55,2 mg/kgBW orally at 24 hours after PMSG administration.
Aquades was administered as a control group. At the age of 30 days, all rats were
sacrificed to make histology and immunohistology samples of the granulosa cells.
Evaluation of COX-2 expression used immunohistochemistry technique with
prime antibody of Rabbit Monoklonal (RB-9072-P) to determine the antigen
location.
Results: The PGV-0 group showed expression of COX-2 lower than the control
group and LH+PGV-0 group. This supports that administration of PGV-0
decreased expression of COX-2 in granulosa cells. LH+teophylline+PGV-0 group
showed expression of COX-2 not lower than LH+teophylline group, on the
contrary this group showed higher expression of COX-2 than teophylline+PGV-0
group, supporting that the action site of PGV-0 is in the downstream cAMP of
cAMP pathway and there were other pathways beside cAMP pathway stimulated
by LH.
Conclusions: The results suggest that PGV-0 inhibited expression of COX-2 in
granulosa cells ovary follicle and the action site of PGV-0 is in downstream
cAMP in cAMP pathway.
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