Xuezhikang, an extract of cholestin, protects endothelial function through antiinflammatory and lipid-lowering mechanisms in patients with coronary heart disease.

BACKGROUND: Endothelial dysfunction is associated with inflammation and postprandial hypertriglyceridemia. Xuezhikang, an extract of Cholestin, a dietary supplement, has lipid-modulating and antiinflammatory effects. We explored the effects of xuezhikang on endothelial function and high-sensitivity C-reactive protein (hs-CRP) in patients with coronary heart disease (CHD). METHODS AND RESULTS: We prospectively randomized 50 CHD patients to xuezhikang 1200 mg/d or placebo for 6 weeks. Fasting hs-CRP concentrations, flow-mediated vasodilation (FMD) at 0 and 4 hours, and lipid parameters at 0, 2, 4, and 6 hours were monitored after a high-fat meal (800 calories; 50 g fat) in all patients. All patients underwent a high-fat meal test at the beginning of the study and after 6 weeks of treatment. Postprandial FMD was significantly worse at 4 hours after a high-fat meal (P<0.05), and this was associated with the area under the triglyceride curve (TG-AUC) (r=0.345, P<0.01). After 6 weeks of xuezhikang, fasting hs-CRP levels and TG-AUC (P<0.001 for each) decreased. Furthermore, preprandial and postprandial FMD significantly improved (P<0.001). There were no significant changes in serum lipids and FMD in the placebo arm. In multivariable regression analysis, changes in TG-AUC and fasting hs-CRP levels were predictive of improvement in preprandial FMD (P<0.05). CONCLUSIONS: Xuezhikang effectively improved preprandial and postprandial endothelial function through its potent antiinflammatory and lipid-lowering effects.

Xuezhikang decreases serum lipoprotein(a) and C-reactive protein concentrations in patients with coronary heart disease.

BACKGROUND: Increased serum lipoprotein(a) [Lp(a)] and high-sensitivity C-reactive protein (hsCRP) concentrations are independent risk factors for coronary heart disease (CHD). Xuezhikang, an extract of cholestin, effectively lowers fasting cholesterol and triglyceride concentrations. We studied whether xuezhikang lowered Lp(a) and hsCRP concentrations. METHODS: We randomly divided 60 CHD patients into two groups to receive xuezhikang (1200 mg daily) or placebo for 6 weeks. The fasting hsCRP concentration and the postprandial changes of serum lipid concentrations at 2, 4, and 6 h after a high-fat meal (800 calories; 50 g of fat) were measured before and after the 6-week protocol. RESULTS: The two groups had similar baseline fasting lipid and hsCRP concentrations. The postprandial triglyceride and Lp(a) concentrations were significantly increased (P <0.05). After 6 weeks, the fasting and postprandial lipid concentrations decreased significantly in the xuezhikang group, accompanied by a significant reduction in fasting hsCRP concentration (P <0.001). The placebo group had no significant change in lipid concentrations, whereas the fasting serum hsCRP concentration was reduced significantly (P <0.05). The reduction in hsCRP was closely related to the changes in fasting Lp(a) concentration (r = 0.402; P <0.05) and triglyceride area under the curve (r = 0.441; P <0.001). CONCLUSIONS: Xuezhikang effectively decreased fasting Lp(a) and postprandial triglyceride concentrations, which were associated with reductions of fasting hsCRP concentrations in CHD patients.

Effect of xuezhikang, a cholestin extract, on reflecting postprandial triglyceridemia after a high-fat meal in patients with coronary heart disease.

The effect of xuezhikang on postprandial triglyceride (TG) level was investigated in patients with coronary heart disease (CHD) after a high-fat meal (800 cal; 50 g fat). Fifty CHD patients were randomly divided into two groups to accept xuezhikang (xuezhikang group) 1200 mg/day (600 mg twice daily) or not (control group) on the base of routine therapy which included aspirin, metoprolol and fosinopril and nitrates during the whole 6 weeks following-up. Xuezhikang significantly reduced fasting serum total cholesterol (TC) (-20%), low-density lipoprotein cholesterol (LDL-C, -34%), TG (-32%) and apoB (-27%) levels, and raised fasting high-density lipoprotein cholesterol (HDL-C, 18%) and apoA-I (13%) levels (P<0.001). The postprandial serum TG levels at 2, 4 and 6 h decreased 32, 38 and 43%, respectively, in xuezhikang group (P<0.001). The TG area under the curve over the fasting TG level (TG-AUC) significantly decreased in CHD patients accepted xuezhikang with normal (less than 1.7 mmol/l) and elevated (1.74 to 2.92 mmol/l) fasting TG levels by 45 and 50%, respectively (P<0.001). Routine therapy had no significant effect on the fasting and postprandial lipid and apolipoprotein levels. The change of TG-AUC was significantly related to the changes of fasting TG, TC, LDL-C, and HDL-C levels after the treatment, which were related to the changes of fasting apoA-I and apoB levels significantly (P<0.001). Xuezhikang was shown to be beneficial in the treatment of reflecting postprandial triglyceridemia in CHD patients with normal and mildly elevated fasting TG levels.

The lipoprotein lipase Ser447Ter mutation and risk of stroke in the Chinese.

BACKGROUND: Lipoprotein lipase (LPL) plays an important role in plasma lipoprotein metabolism. The Ser447Ter mutation of LPL may be associated with ischemic cerebrovascular diseases. We investigated whether the LPL variants were related to risk of strokes in Chinese Hans. METHODS: We recruited 160 patients with cerebrovascular diseases (ischemic stroke, n=96; hemorrhagic stroke, n=64) and 117 age-matched controls. All subjects were Chinese Hans. Subjects were analyzed for the Ser447Ter mutation by restriction fragment length polymorphisms of the LPL gene. RESULTS: As compared with controls, the frequency of LPL genotype CG (heterozygous Ser447Ter mutation) was lower in ischemic stroke patients (10.4% vs. 21.4%, p<0.05), and was not significantly different in hemorrhagic stroke patients (15.6% vs. 21.4%, p>0.05). The LPL G allele frequency was also lower in ischemic stroke patients (5.2%) vs. controls (10.7%, p<0.05). There was no difference between hemorrhagic stroke patients (7.8%) and controls. Serum Lp(a) concentrations were markedly lower in CG carriers than that in CC carriers in both stroke patients and the controls (p<0.05). There was no significant difference in the concentrations of other lipids. CONCLUSIONS: Patients with ischemic stroke have a lower frequency of the LPL Ser447Ter mutation, which indicates that this mutation may have protective effect on ischemic stroke.