ABSTRACT
Objective: To observe the clinical effect and protection of vascular endothelium of SoftenClean Capsule (SCC) in middle-aged and senior people with unstable angina and hyperlipidemia. Methods: Six hundred and fifty patients with unstable angina were randomly divided into SCC group (340 cases) and control group (310 cases). Conventional statin therapy was given to both groups, with SCC group receiving additional SCC treatment. Data of 216 healthy persons were taken as normal group. Also one hundred and forty-eight patients with hyperlipidemia were taken from SCC group (treated with SCC) and 170 from control group (treated with Simvastatin) respectively. The changes of clinical symptoms and laboratory indexes in all the patients were observed before and after treatment. Results: In patients with unstable angina, the efficacy of treatment of SCC, the withdrawal rate of nitroglycerin, the relieving of symptoms, the improvement of the electrocardiogram, the counts of circulating endothelial cells, the content of platelet P-selectin, the content of plasma endothelin (ET), the activity of superoxide dismutase (SOD) and the activity of malonyldialdehyde (MDA) were all better than those in the control group. In patients with hyperlipidemia, there was significant difference in lipids reduction between SCC group and the control group. In both groups, the total cholesterol (TC), triglyceride (TG), low density lipo-protein-cholesterol (LDL-C), lipoprotein(a) [Lp(a)], ET, oxidized low density lipoprotein, MDA, arteriosclerotic index (AI) all lowered obviously, while the SOD, HDL-C and calcitonin gene-related peptide (CGRP) were all elevated markedly. In the SCC group, the nitric oxide (NO) increased significantly whereas the ET/CGRP and ET/NO decreased markedly. The total effective rate in symptom relieving, the markedly effective rate, the reduction of TC, ET and ET/CGRP, and the elevation of SOD in SCC group were all superior to those in the control group. Conclusion: SoftenClean Capsule could effectively resist myocardial ischemia, relieve angina, reduce blood lipids, protect vascular endothelial cells, inhibit the activation of platelets, and resist lipid peroxidation.
KEY WORDS: unstable angina, hyperlipidemia, SoftenClean capsule, protection of vascular endothelium, therapy of traditional herbal medicine
The etiology and pathogenesis of hyperlipidemia and CHD in middle-aged and senior people are mostly attributed to deteriorated functions of internal organs especially heart, spleen and kidney. Hyperlipidemia generally originates from insufficiency of the spleen function and defect in oxygen and nutrient transportation and transformation, and is manifested by phlegm and blood stasis in the interior circulation system. Unstable angina that results from blood stasis and phlegm in heart channels is characterized by “insufficiency of metabolism in the heart and spleen organs”. SCC consists of ginseng, Ginkgo leaf, notoginseng, extracts from green tea and taurine. Its function is to “replenish energy, nourish the heart, invigorate the spleen and kidney, promote blood circulation to remove obstruction in the circulation system, resolve phlegm and remove turbidity”. It acts in coordination to invigorate spleen/kidney and remove plaque clots and cures both the root causes and the symptoms, which is the very thing needed for the pathogenesis of the two above-mentioned diseases.
Modern pharmacological study has demonstrated that each ingredient has anti-myocardial ischemia, hyperlipidemia-lowering, anti-oxidation and vascular endothelium protection effects. With its remarkable holistic potencies, it could play a vital role in clinical applications. Therefore, SCC has obtained satisfactory results for both unstable angina and hyperlipidemia, not only in improving hyperlipidemia dramatically, in relieving angina and in getting beneficial response to ECG, but also in ameliorating clinical symptoms.
Vascular endothelial cells (VEC) are the first permeability barrier between vascular walls and blood. It could synthesize and secrete a variety of endothelium-derived vasoactivators such as ET, NO, maintain the stability of ET/NO, ET/CGRP and modulate the contraction and dilation of blood vessels by regulating vascoactive substances. Hyperlipidemia, vascular endothelium injury and angina pectoris are closely interrelated. VEC injury is a vital and initial factor in arteriosclerosis (AS). In the case of hyperlipidemia, high levels of TC, free radicals, LDL and OX-LDL in blood may cause damage to VEC. The lipid peroxidation reaction triggered by oxygen free radicals is an important mechanism of the endothelial injury. OX-LDL produced by oxidative-modification has a toxic effect on VEC, which leads to obvious damage and plays an active role in the formation of AS. The vascular endothelial injury is closely related to the formation and rupture of unstable AS plaque as well as thrombosis and coronary spasm, which is of vital importance to the pathogenesis of unstable angina. The abnormal elevations of ET/CGRP and ET/NO in the presence of vascular endothelial injury reflect the severity of VEC injury. CEC is now considered as the sole indicator of VEC injury specifically and directly (6).
The results showed that CEC and ET in both groups with unstable angina before treatment were much higher than those in the normal group, whereas NO was markedly lower than that in the normal group, which could serve as evidence of the vascular endothelial injury. In addition, in the patients with hyperlipidemia, SCC could increase CGRP and NO significantly,
and lower ET, ET/CGRP and ET/NO. In the patients with unstable angina SCC could drastically decrease CEC and ET, but elevate NO. This indicated that SCC could inhibit the disturbance of the secretion of VEC, alleviate the VEC injury and have a remarkable protective effect on VEC. Moreover, SCC could elevate the activity of SOD and lower the content level of MDA and OX-LDL. This suggested that SCC could enhance the anti-oxidation, relieve the lipid peroxidation injury and inhibit the oxidative-modification of lipoproteins. The mechanism that SCC could protect the vascular endothelium is related to hyperlipidemia-lowering, elevation of HDL-C, reduction of LDL-C and OX-LDL, and anti-oxidation.
Platelet activation is the initial link of thrombosis of unstable angina. CD62p, also known as GMP-140 and mainly expressed on the surface of activated platelets and VEC, could mediate the adhesion between VEC and inflammatory cells as well as between platelets, monocytes and neutrophils, and therefore could give rise to functional disturbance and injury of VEC, and thus it is used as one of the principal markers in platelet activation. This study revealed that the content of CD62p in the patients with unstable angina increased significantly and after treatment with SCC decreased markedly, which is much better than that in the control group. This showed that SCC has the effect of inhibiting platelet activation, helps protect vascular endothelium and alleviates thrombosis and vasospasm induced by rupture of AS plaque. This could be a main pathogenetic factor in treating unstable angina.
Lp (a) has been regarded as an independent, important risk factor in causing AS. The high level of Lp(a) in blood is likely to induce AS by affecting the metabolism of cholesterol and fibrinolysis (7). Compared with after treatment between two groups, the remarkable effect of SCC in reducing Lp(a) helps to reverse and regress AS.
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