OBJECTIVE: To investigate the changes in contents of cycloxygenase-2 (COX-2) and its downstream effectors in rat's myocardial ischemia/reperfusion (I/R) model and observe the effects of precondition with GBE50 (Ginkgo biloba extract 50) and Salviae miltiorrhizae (SM) on them. METHODS: Rat's I/R model was established by 30-min left anterior descending coronary artery occlusion followed with 60-min reperfusion. Animals were divided into the model control group, the sham-operated group and the tested groups (received 1-week precondition with GBE50 and SM respectively via intragastric infusion before modeling). COX-2 mRNA expression in myocardium was detected by real-time PCR; contents of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) were measured by radioimmunoassay. RESULTS: The mRNA expression of COX-2 in the model group was obviously higher than that in the sham-operated group (P < 0.001), while that in the tested groups was down-regulated significantly (P < 0.01), and the content of TXB2 as well as the ratio of TXB2/PGF1alpha was reduced significantly (P < 0.05). Besides, SM also showed the up-regulation effect on 6-keto-PGF1alpha content in myocardium (P < 0.05). CONCLUSION: COX-2 affects the myocardium through thromboxane A2 and prostacyclin after I/R; both GBE50 and SM can inhibit the production of COX-2, but they may act in different paths.
OBJECTIVE: To investigate the changes in contents of cycloxygenase-2 (COX-2) and its downstream effectors in rat's myocardial ischemia/reperfusion (I/R) model and observe the effects of precondition with GBE50 (Ginkgo biloba extract 50) and Salviae miltiorrhizae (SM) on them. METHODS:Rat's I/R model was established by 30-min left anterior descending coronary artery occlusion followed with 60-min reperfusion. Animals were divided into the model control group, the sham-operated group and the tested groups (received 1-week precondition with GBE50 and SM respectively via intragastric infusion before modeling). COX-2 mRNA expression in myocardium was detected by real-time PCR; contents of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) were measured by radioimmunoassay. RESULTS: The mRNA expression of COX-2 in the model group was obviously higher than that in the sham-operated group (P < 0.001), while that in the tested groups was down-regulated significantly (P < 0.01), and the content of TXB2 as well as the ratio of TXB2/PGF1alpha was reduced significantly (P < 0.05). Besides, SM also showed the up-regulation effect on 6-keto-PGF1alpha content in myocardium (P < 0.05). CONCLUSION: COX-2 affects the myocardium through thromboxane A2 and prostacyclin after I/R; both GBE50 and SM can inhibit the production of COX-2, but they may act in different paths.