Therapeutic Effect and Mechanism of Action of Abnormal Savda Munziq in Development of Degenerative Atherosclerotic Aortic Valve Disease.

BACKGROUND The aim of this study was to investigate the therapeutic effect of abnormal Savda Munziq (ASMq) on the development of degenerative atherosclerotic aortic valve disease and its underlying mechanisms. MATERIAL AND METHODS We randomly divided 80 rabbits into 4 groups: a normal control group (group N, n=20); a high-fat diet group (group HC, n=20); a high-fat diet and Atorvastatin calcium intervention group (group AI, n=20); and a high-fat diet and ASMq intervention group (group MI, n=20). For evaluation of blood lipid profiles, blood samples were collected at week 0 and at the end of week 8. Aortic valve samples were taken at weeks 0, 2, 4, 6, and 8 for atomic force microscopy (AFM) examination of endothelial cell nanostructures, and at week 8 for pathological examinations. RESULTS Triglyceride (TG), cholesterol (TC), low-density lipoprotein (LDL), and high-density lipoprotein HDL levels of rabbits in group HC were significantly different from those in group N (P<0.01). TG, TC, LDL, and HDL values of rabbits in group MI were significantly different from rabbits in group HC (P<0.05). Pathological examination revealed that the aortic valves from rabbits in group MI were visibly clear, with strong endothelial cell continuity. No infiltration of macrophages or other inflammatory cells nor subendothelial calcium deposition was found when compared with rabbits in group HC. CONCLUSIONS ASMq therapy can delay the onset of degenerative calcific aortic valve disease, and its effects are similar to those of Atorvastatin.

[Establishment of Uyghur Medicine Abnormal Savda Carrier MIRI Animal Model and its Cardiac Ultrastructural Changes].

OBJECTIVE: To innovatively establish a new platform of myocardial ischemia-reperfusion injury (MIRI) animal model by observing abnormal savda carrier MIRI indicators, and to observe changes of myocardial ultrastructure. METHODS: According to Uyghur medical theories, an abnormal savda carrier animal model was established and confirmed using multifactor, and then MIRI models set up. Totally 36 male white SD rats were randomly divided into the normal sham-operation group, the normal operation group, the model sham-operation group, and the model operation group, 9 in each group. ECG changes, myocardial enzymes (CK-MB), and cardiac troponin (cTnT), and ultramicrostructures were observed. RESULTS: Compared with the normal sham-operation group, some damage of ultramicrostructures occurred in heart muscles of rats in the normal operation group and the model operation group, such as lowered myoplasm density, loosely arranged myofilament, dilated myofibris, reduced mitochondria number, vacuole and swelling mitochondrion. Ultramicrostructural damage of cardiac muscle cells was more severe in rats of the model operation group. Compared with the normal sham-operation group, CK-MB and cTnT increased in the normal operation group with statistical difference (P < 0.01). Compared with the normal sham-operation group, there was no statistical difference in CK-MB or cTnT in the model sham-operation group (P > 0.05). Compared with the model operation group, CK-MB and cTnT obviously decreased in the model sham-operation group and the normal operation group with statistical difference (all P < 0.01). CONCLUSION: Abnormal savda carrier MIRI model established in this experiment could provide favorable conditions for further MIRI intervention treatment.

Inhibition of nuclear factor kappa B pathway protects myocardial ischemia/reperfusion injury in rats under treatment with abnormal savda munziq.

OBJECTIVE: Uighur medicine Fufang Munziq granule (Munziq) [corrected] shows cardioprotective effect in myocardial ischemia/reperfusion injury (IRI) in animal models, but the molecular mechanism of this effect is not clear. The present study investigates the regulation of nuclear factor kappa B (NF-kappa B) pathway by Fufang Munziq granule (Munziq) in IRI rat models. METHODS: Male Sprague-Dawley rats were divided into three groups: the NF-κB gene knockout group (n = 5); the NF-κB transgenic group (n = 8); and the control group (n = 5). All rats were treated with Fufang Munziq granule (Munziq) [corrected] for 21 days before underwent IRI surgical procedure. Blood and tissue samples were collected for the RT-PCR, ELISA, western blot and other examination. RESULTS: Expression of NF-κB p65mRNA and protein were down-regulated in the NF-κB knockout rats but up-regulated in the transgenic rats comparing with the controls (P<0.05). The upstream NF-κB kinase expressions, the downstream inflammatory cytokines, and the myocardial injury markers were all changed in accordance with the NF-κB gene modification (all P values <0.05). AMSq treatment relieved IRI in the NF-κB knockout rats. CONCLUSION: Inhibition on NF-κB signaling pathway may alleviate IRI in rats under Fufang Munziq granule (Munziq) [corrected] treatment.

Erratum: Inhibition of nuclear factor kappa B pathway protects myocardial ischemia/reperfusion injury in rats under treatment with Fufang Munziq granule (Munziq).

[This corrects the article on p. 77 in vol. 10, PMID: 29422995.].