Hypolipidemic activity of a hydroalcoholic extract of Cyperus scariosus Linn. root in guinea pigs fed with a high cholesterol diet

Lipid-lowering and antioxidant activities of a hydroalcoholic extract of Cyperus scariosus Linn. root（HCS） were evaluated in guinea pigs fed with a high cholesterol diet. Serum lipid profile（total cholesterol, triglycerides, LDL-C, VLDL-C, and HDL-C）, atherogenic indices and serum enzymes（ALT, AST, ALP, LDH, and CK-MB） were performed in each group at 0 days and at the end of 60 days. Histological study of liver and kidney was done in groups 1, 2, 5, 6 and 7. The total phenolic and flavonoid content in HCS and its antioxidant activity were evaluated by the DPPH assay. Both doses of HCS decreased serum lipid profile and atherogenic indices（P 〈 0.05）. HCS has lipid lowering, immunosuppressive and antioxidant properties, and mays have value in atherosclerosis prevention. The higher dose of HCS also reduced serum AST, ALP, and LDH levels and rosuvastatin increased AST and ALP levels（P 〈 0.05）. Histology of the liver showed decreased lipid accumulation and improvement in hepatocytes in HCStreated animals. The antioxidant activity of HCS may be responsible for its lipid lowering and cytoprotective action. HCS had significant lipid lowering and antioxidant activity, which; may be due to the phenolic compounds. HCS may be a safe and cost effective alternative to current statin therapy for patients with dyslipidaemia.     

普伐他汀、福辛普利及合用对大鼠心肌梗死后肿瘤坏死因子-α表达及心室重构的影响

目的探讨普伐他汀、福辛普利及合用对大鼠心肌梗死后心室重构、心功能、肿瘤坏死因子α(TNFα)表达、基质金属蛋白酶(MMPs)活性等的影响。方法通过结扎冠状动脉前降支诱导大鼠急性心肌梗死(AMI),AMI后24h存活的48只大鼠随机分为AMI组,福辛普利组(10mg·kg1·d1),普伐他汀组(20mg·kg1·d1),普伐他汀(20mg·kg1·d1)加福辛普利组(10mg·kg1·d1),每组12只。另设假手术组(n=8)。术后24h开始直接灌胃给药,AMI及假手术组大鼠灌等量生理盐水。用药42天后,测定心功能和血流动力学参数,以反转录聚合酶链反应检测心肌TNFαmRNA的表达,酶谱法测定左室心肌MMPs活性,并测定心室重量/体重。结果梗死面积在AMI及各治疗组间差异均无统计学意义。与AMI组比较,福辛普利、普伐他汀、联合用药均使AMI组增加的左室舒张末压、左室舒张末直径、左室相对重量下降(P<0.05～0.01),使下降的左室压最大上升速率和下降速率、左室短轴缩短率、射血分数不同程度增加(P<0.05～0.01)。福辛普利、普伐他汀、联合用药分别使AMI组表达增加的TNFα降低29%、26%、33%(P<0.01);使MMP2活性水平降低25%、30%、35%(P<0.01);使MMP9活性水平降低20%、18%、24%(P<0.01)。联合用药较单用福辛普利或普伐他汀,对射血分数、左室短轴缩短率、左室压最大上     

Long-term effect of low-density lipoprotein apheresis in patients with heterozygous familial hypercholesterolemia

Clinical efficacy and safety of the therapeutic tool which directly removes LDL particles from circulation (LDL apheresis) have already been established in the treatment for refractory hypercholesterolemia in patients with familial hypercholesterolemia (FH). Two clinical studies with event-based assessment have demonstrated remarkably beneficial outcomes of long-term LDL apheresis using dextran sulfate cellulose columns plus adjunctive cholesterol-lowering drug therapy in the prevention of cardiovascular events in heterozygous FH with coronary artery disease. The results of several studies with angiographic and ultrasound-based assessment indicate a possible role for LDL apheresis in restructuring and stabilization of atherosclerotic lesions. These clinical improvements caused by LDL apheresis in heterozygous FH support the efficacy and importance of aggressive cholesterol-lowering therapy for secondary prevention of atherosclerotic cardiovascular disease in hypercholesterolemic patients.     

Simvastatin reduces plasma concentration of high-sensitivity C-reactive protein in type 2 diabetic patients with hyperlipidemia

High-sensitivity C-reactive protein (hs-CRP) is positively associated with the prevalence of coronary artery disease by epidemiologic data. Prospective studies indicate that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors reduced the plasma hs-CRP concentration and the risk of recurrent coronary events after myocardial infarction. Type 2 diabetes is associated with high mortality risk of coronary heart disease and this high risk may be involved in the inflammatory factors. We have therefore conducted a prospective study to assess whether simvastatin can rapidly reduce the plasma hs-CRP concentration in type 2 diabetic patients with hyperlipidemia. Seventeen type 2 diabetic patients with hyperlipidemia were enrolled in the study after 6 weeks on a lipid-lowering diet. Fourteen patients completed the study, taking simvastatin 20 mg daily for 8 weeks. Fasting blood samples were collected from each patient before and after 8-week administration of simvastatin. In response to 8-week administration of simvastatin, hs-CRP levels significantly decreased from 0.312±0.057 to 0.193±0.045 mg/dl (P<.01). Plasma LDL cholesterol also decreased significantly from 130±9 to 74±3 mg/dl (P=.001). This study shows that plasma hs-CRP concentration can be reduced by 8-week administration of simvastatin in type 2 diabetic patients with hyperlipidemia.     

Changes of Lipid Profile and C-Reactive Protein after Withdrawal of Xuezhikang,an Extract of Cholestin,in Patients With Stable Angina Pectoris

Lipid-lowering therapy using HMG-CoA reductase inhibitors (statins) has been shown to assist in the prevention of cardiovascular events in many clinical trials[1-3]. Statins may also have an abundance of pleiotropic effects[4-7]. C-reactive protein (CRP),…     

Effects of Statins on High-Density Lipoproteins: A Potential Contribution to Cardiovascular Benefit

PURPOSE: The objective was to systematically review clinical trial data on the effects of statins on high-density lipoproteins (HDL) and to examine the possibility that this provides cardiovascular benefits in addition to those derived from reductions in low-density lipoproteins (LDL). METHODS: The PubMed database was searched for publications describing clinical trials of atorvastatin, pravastatin, rosuvastatin, and simvastatin. On the basis of predefined criteria, 103 were selected for review. RESULTS: Compared with placebo, statins raise HDL, measured as HDL-cholesterol (HDL-C) and apolipoprotein A-I (apo A-I); these elevations are maintained in the long-term. In hypercholesterolemia, HDL-C is raised by approximately 4% to 10%. The percentage changes are greater in patients with low baseline levels, including those with the common combination of high triglycerides (TG) and low HDL-C. These effects do not appear to be dose-related although there is evidence that, with the exception of atorvastatin, the changes in HDL-C are proportional to reductions in apo B-containing lipoproteins. The most likely explanation is a reduced rate of cholesteryl ester transfer protein (CETP)-mediated flow of cholesterol from HDL. There is some evidence that the statin effects on HDL reduce progression of atherosclerosis and risk of cardiovascular disease independently of reductions in LDL. CONCLUSION: Statins cause modest increases in HDL-C and apo A-I probably mediated by reductions in CETP activity. It is plausible that such changes independently contribute to the cardiovascular benefits of the statin class but more studies are needed to further explore this possibility.     

Association between statin use and cognitive function: A systematic review of randomized clinical trials and observational studies

The US Food and Drug Administration issued a black box warning in 2012 regarding the association of statin use with cognitive impairment. This may deter patients and practitioners from using statins for guideline-directed indications. Large studies have not shown an increase in cognitive impairment with statin use. MEDLINE, EMBASE, and Cochrane databases were searched up to October 2019. We present an up-to-date systematic review of randomized controlled trials (RCTs) and prospective observational studies examining the association between statin use and cognitive status in a population aged ≥60 years. Twenty-four studies with 1,404,459 participants were included in the review. Twenty-one were prospective observational studies, and 3 were RCTs. All 3 RCTs, which ranged from 3.2 to 5.6 years of follow-up, showed no significant association between statin use and adverse cognitive effects (odds ratio [OR] 1.03 [0.82–1.30]) and (OR 1.0 [0.61–1.65]). The mean difference in the Mini-Mental State Examination was insignificant (0.06 [?0.04 to 0.16]) in the third RCT. The follow-up for observational studies ranged from 3 to 15 years. Ten observational studies showed reduced incidence of dementia. Seven showed no association with incident dementia. Three studies showed decline in cognition was similar, whereas one showed slower decline with statin use. There was no evidence of adverse cognitive effects, including incidence of dementia, deterioration in global cognition, or specific cognitive domains associated with statin use in individuals aged ≥60 years. Future studies should examine this association in studies with longer follow-up periods.     

Impact of prior statin use on clinical outcomes in COVID-19 patients: data from tertiary referral hospitals during COVID-19 pandemic in Italy

BackgroundEpidemiological evidence suggests that anti-inflammatory and immunomodulatory properties of statins may reduce the risk of infections and infection-related complications.ObjectiveWe aimed to assess the impact of prior statin use on coronavirus disease (COVID-19) severity and mortality.MethodsIn this observational multicenter study, consecutive patients hospitalized for COVID-19 were enrolled. In-hospital mortality and severity of COVID-19 assessed with National Early Warning Score (NEWS) were deemed primary and secondary outcomes, respectively. Propensity score (PS) matching was used to obtain balanced cohorts.ResultsAmong 842 patients enrolled, 179 (21%) were treated with statins before admission. Statin patients showed more comorbidities and more severe COVID-19 (NEWS 4 [IQR 2–6] vs 3 [IQR 2–5], p < 0.001). Despite having similar rates of intensive care unit admission, noninvasive ventilation, and mechanical ventilation, statin users appeared to show higher mortality rates. After balancing pre-existing relevant clinical conditions that could affect COVID-19 prognosis with PS matching, statin therapy confirmed its association with a more severe disease (NEWS ≥5 61% vs. 48%, p = 0.025) but not with in-hospital mortality (26% vs. 28%, p = 0.185). At univariate logistic regression analysis, statin use was confirmed not to be associated with mortality (OR 0.901; 95% CI: 0.537 to 1.51; p = 0.692) and to be associated with a more severe disease (NEWS≥5 OR 1.7; 95% CI 1.067–2.71; p = 0.026).ConclusionsOur results did not confirm the supposed favorable effects of statin therapy on COVID-19 outcomes. Conversely, they suggest that statin use should be considered as a proxy of underlying comorbidities, which indeed expose to increased risks of more severe COVID-19.