Anti-inflammatory Therapy Progress in Major Adverse Cardiac Events after PCI: Chinese and Western Medicine.

Acute coronary syndrome (ACS) is one of the leading causes of death in cardiovascular disease. Percutaneous coronary intervention (PCI) is an important method for the treatment of coronary heart disease (CHD), and it has greatly reduced the mortality of ACS patients since its application. However, a series of new problems may occur after PCI, such as in-stent restenosis, no-reflow phenomenon, in-stent neoatherosclerosis, late stent thrombosis, myocardial ischemia-reperfusion injury, and malignant ventricular arrhythmias, which result in the occurrence of major adverse cardiac events (MACE) that seriously reduce the postoperative benefit for patients. The inflammatory response is a key mechanism of MACE after PCI. Therefore, examining effective anti-inflammatory therapies after PCI in patients with ACS is a current research focus to reduce the incidence of MACE. The pharmacological mechanism and clinical efficacy of routine Western medicine treatment for the anti-inflammatory treatment of CHD have been verified. Many Chinese medicine (CM) preparations have been widely used in the treatment of CHD. Basic and clinical studies showed that effectiveness of the combination of CM and Western medicine treatments in reducing incidence of MACE after PCI was better than Western medicine treatment alone. The current paper reviewed the potential mechanism of the inflammatory response and occurrence of MACE after PCI in patients with ACS and the research progress of combined Chinese and Western medicine treatments in reducing incidence of MACE. The results provide a theoretical basis for further research and clinical treatment.

[Terpenoids isolated from Viburnum ternatum].

Four iridoids (1-4), five iridoid glucosides (5-9), and three triterpenoids (10-12) were isolated from the ethyl acetate soluble fraction of 70% Me2CO extract of the aerial parts of Viburnum ternatum through various column chromatographies over silica gel, ODS, Sephadex LH-20 and MCI. Their structures were elucidated as ternatumin A (1), 2,9-dioxatricyclo[4.3.1.03，7]decanes (2), 7,10,2'-triacetylsuspensolide F (3), 7,10,2',3'-tetraacetylsuspensolide F (4), viburtinoside IV (5), viburtinoside II (6), viburtinoside B (7), luzonoside A (8), luzonoside B (9), 2α,3ß,24-trihydroxy-12-ursen-28-oic acid (10), 6-hydroxy-20(29)-lupen-3-one (11), and pomalic acid (12) based on the their chromatographic properties, chemical and physicochemical methods, and spectroscopic data. Compound 1 was a new compound and compounds 3-12 were isolated from this plant for the first time. Furthermore, we note here the first isolation of compound 2 as a new natural product.

[Protective effects of hydroxyethylpuerarin against brain astrocytes injury induced by hydrogen peroxide].

AIM: To study the protective effects of hydroxyethylpuerarin against the injury of astrocytes induced by hydrogen peroxide (H2O2). METHODS: Experiments were performed with cells from passage 4. Plasma membrane integrity was measured by lactate dehydrogenase (LDH) release. The occurrence of apoptosis was measured by flow cytometry. The glutamate uptake of astrocytes was studied with [3H]-glutamate incorporation. Intracellular superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were assessed by automatic biochemistry analyzer. RESULTS: Compared with H2O2 injured group, the occurrence of apoptosis, levels of LDH release and intracellular MDA of astrocytes reduced in hydroxyethylpuerarin pre-treated groups, but the glutamate uptake and intracellular SOD activity of astrocytes increased. CONCLUSION: Hydroxyethylpuerarin could reduce the occurrence of apoptosis and improve neurotrophic function of astrocytes, which may be related with its antioxidant effects during oxidative stress.

Protective effects of hydroxyethylpuerarin on cultured bovine cerebral microvascular endothelial cells damaged by hydrogen peroxide.

AIM: To observe the damages induced by hydrogen peroxide in cultured bovine cerebral microvascular endothelial cells (BCMEC) and evaluate the protective effects of hydroxyethylpuerarin on hydrogen peroxide-injured BCMEC. METHODS: BCMEC were cultured and transferred into modified Eagle medium (MEM). The viability of cells was detected by MTT assay. Cell injury was determined by lactate dehydrogenase (LDH) activity in the extracellular medium. Flow cytometry was employed to observe the occurrence of apoptosis. Morphologic changes of cells were visualized under phase contrast and electron microscopes. RESULTS: Hydrogen peroxide (200 micromol x L(-1) for 4 hours) inhibited the viability of cultured BCMEC and stimulated LDH release. Hydrogen peroxide (100 micromol x L(-1) for 4 hours) induced the occurrence of apoptosis. Hydroxyethylpuerarin was shown to increase the survival rate and decrease the activity of LDH of BCMEC damaged by hydrogen peroxide. Hydroxyethylpuerarin was also found to protect BCMEC against apoptosis induced by hydrogen peroxide. CONCLUSION: Hydrogen peroxide induces BCMEC injury either by apoptosis or through necrosis. Hydroxyethylpuerarin protects BCMEC against hydrogen peroxide-induced injury in a concentration-dependent manner. Its antioxidant effects might be involved as the mechanism protection.

Serratane-type triterpenoids from Huperzia serrata.

Sixteen serratane-type triterpenoids including three new compounds, 14beta,15beta-epoxyserratan-3beta,21beta,29-triol (1), serrat-14-en-3beta,21beta,29-triol (2) and serrat-14-en-3alpha,21beta,24,29-tetraol (3), were isolated from the whole plant of Huperzia serrata (Thunb) Trev. The structures of these new compounds (1-3) were elucidated on the basis of spectral analysis.