ABSTRACT
Autophagy is a basic process of eliminating unnecessary or damaged organelles by lysosome to maintain the internal environment homeostasis. Recent studies have revealed that autophagy plays an important role in pathology of myocardial ischemia reperfusion. In the phase of ischemia, moderate autophagy can protect the cells against various stress; but in the phase of reperfusion, excessive autophagy can increase the death of cells. Therefore, the dual role of autophagy in myocardial ischemia reperfusion provides a new therapeutic target for the treatment of heart disease. In recent years, more and more Chinese medicines have been proved to adjust the autophagy in myocardial cells, and protect the damaged myocardium by enhancing or inhibiting autophagy. This article would review the molecular mechanisms of autophagy and its role in myocardial ischemia reperfusion injury as well as the regulation effect of Chinese medicine on it.
ABSTRACT
Mitochondria is the key energy source of cells and plays an important role in energy synthesis and release, and maintenance of cellular functions. As the most important active ingredients in Chinese medicine pseudo-ginseng, Panax notoginseng saponins(PNS) have pharmacological effects on protecting against thrombosis, dilating blood vessels, lowering the blood pressure, anti-inflammation, and antioxidant, etc. Domestic and foreign studies have shown that PNS participates in regulating mitochondrial energy metabolism, oxidative stress, biosynthesis, apoptosis, mitophagy and the status of membrane channels. Therefore, the mitochondria is one of the important targets of PNS. In this paper, the regulation effects of P. notoginseng saponins on mitochondria were reviewed.
ABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>