Objective To systematically evaluate the safety of high dose atorvastatin (80 mg daily) in Chinese patients. Methods Randomized controlled trials (RCTs) investigating 80 mg/ d atorvastatin vs. low-dose atorvastatin or placebo or blank were electionically retrieved in date bases of EMbase, PubMed, the Cochrane Library, WanFang, CNKI and WeiPu. Meta-analysis was performed using RevMan 5. 2 and Stata 11. 0 software. Results A total of 20 RCTs involving 2282 cases were included. The results of meta-analysis showed no significant differences betweent the 80 mg/ d atorvastatin group and the control group in the incidence of gastrointestinal adverse events (RR 1. 53, 95% CI 0. 85-2. 76, P = 0. 16), hepatic adverse events (RR 1. 53, 95% CI 0. 99 - 2. 36, P = 0. 05), muscular adverse events (RR 1. 51, 95% CI 0. 92 -2. 49, P = 0. 10), serious hepatic injuries ( RR 2. 33,95% CI 0. 88 - 6. 20, P = 0. 09) and serious muscular myopathies (RR 1. 40, 95% CI 0. 46 - 4. 30, P = 0. 56). Subgroup analysis by type of cotrast media used and durations of taking 80 mg/ d atorvastatin showed there were higher risks of gastrointestinal adverse events in the 80 mg/ d group when compared to blank control ( RR 4. 22, 95% CI 1. 11 - 16. 04, P = 0. 03). Conclusions The current evidence shows that 80 mg / d atorvastatin may be relatively safe in terms of adverse events in gastrointestinal tract, liver and muscular system, and relatively has risk in causing severe liver injuries and myopathies. With limited quantity and quality from the RCTs available, more high quality RCTs are needed to verify the above conclusion.

Objective To examine the effect function of platelet(Pt)assemble rate(PLTAR) and the change of protein kinase B(PKB) active by cilostazol (CS)and aspirin (AS)on elderly patients with acute coronary sydrome(ACS). Methods Forty-eight elderly patients with ACS were divided randomly into two groups:CS group (100 mg,n=26),AS group (300 mg,n=22).Twenty-six healthy elderly were into the group of normal control(NC group) . The CS group and AS group were treated by routine anticoagulation and antiplatelet.PLTAR and PKB activity were measured at 10 minutes before treatment and at 7 days after treatment 3.5,6.0,24.0 hours. Results The maximum PLTAR in elderly CS group and AS group was elevated significantly compared with NC group(P

Objective:To investigate the protective mechanism of sevoflurane inhalation anesthesia on neurological function in rats with cerebral infarction.Methods:Sixty SD rats were randomly and equally divided into the sham group, cerebral obstruction group, and sevoflurane post conditioning group (Sevo group). Rats in the cerebral obstruction group and Sevo group were underwent wire embolization to establish permanent focal cerebral ischemia rat model. Rats in the sham group were not treated with wire embolization. Rats in the Sevo group received sevoflurane at a volume fraction of 2.5% immediately after reperfusion and were maintained with oxygen for 30 min with 1 L/min oxygen flow. Rats in the sham and cerebral obstruction group received 30 min of continuous oxygen inhalation with 1 L/min oxygen flow. After 24 h, modified neurological deficit bisection (mNSS) was used to assess the neurological function of the rats in the three groups. After that, blood was taken and the rats were sacrificed, and their brain tissues were collected to determine the level of cerebral infarction volume, apoptosis rate, and the levels of serum inflammatory factors, including interleukin (IL)-6, IL-10, IL-1β and tumor necrosis factor-α (TNF-α), as well as malondialdehyde (MDA) levels, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in brain tissue. Toll like receptor 4 (TLR4) and nuclear transcription factor κB (NF-κB) p65 protein expression levels in rat brain tissues were determined by Western blot analysis.Results:In the Sevo group, the mNSS score, cerebral infarct volume ratio, apoptosis rate, IL-6 level, IL-1β level, TNF-α level, MDA level as well as the expression levels of TLR4 and NF-κB p65 in the brain tissues were higher than those of the sham group (all P<0.05) and lower than those of the cerebral obstruction group (all P<0.05). In the Sevo group, IL-10 level as well as SOD and GSH-Px activities were lower than those of the sham group (all P<0.05) and higher than those of the cerebral obstruction group (all P<0.05). Conclusions:Sevoflurane has a certain protective effect on the brain tissue and neurological function of rats with cerebral infarction. This protective effect may be achieved by inhibiting the inflammatory response mediated by the TLR4/NF-κB signal channel, reducing the release of inflammatory factors, reducing inflammation and oxidative stress, and inhibiting cell apoptosis.

OBJECTIVETo investigate the effect of astragaloside IV (As IV) on the activation of rennin-angiotensin system in rats with pressure-overload induced cardiac hypertrophy.

METHODLeft ventricle hypertrophy was induced by abdominal aorta banding between bilateral renal aortas for 12 weeks. Rats were given astragaloside IV 1.0 mg x kg(-1) and 3.3 mg x kg(-1) for 12 weeks, respectively. After treatment, the left ventricular mass index (LVMI)was calculated by morphometry methods. Plasma and cardiac tissue angiotensin II, and plasma aldosterone were measured by ELISA method. Gene expressions of ACE, AT1 and AT2 in cardiac tissue were detected by real time PCR. Protein expressions of AT1 and AT2 in cardiac tissue were detected by Western blot.

RESULTCompared with model rats, LVMI was decreased by astragaloside IV treatment. Biochemical results indicated that the contents of angiotensin II in plasma and cardiac tissue as well as aldosterone in plasma were all increased in abdominal aorta banding rats comparing with sham-operated rats, then, decreased by astragaloside IV treatment. Gene expressions of cardiac ACE was downregulated by astragaloside IV, however, gene and protein expressions of cardiac AT2 were upregulated by astragaloside IV. Both elevated gene and protein expressions of AT1 were not attenuated by astragaloside IV.

CONCLUSIONExcessive activated rennin-angiotensin system in rats with pressure-overload induced cardiac hypertrophy is inhibited by astragaloside IV treatment.

Aldosterone ; blood ; Angiotensin II ; blood ; metabolism ; Animals ; Blood Pressure ; physiology ; Cardiomegaly ; drug therapy ; Enzyme-Linked Immunosorbent Assay ; Hypertrophy, Left Ventricular ; drug therapy ; metabolism ; Male ; Peptidyl-Dipeptidase A ; genetics ; Polymerase Chain Reaction ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 ; genetics ; Receptor, Angiotensin, Type 2 ; genetics ; Renin-Angiotensin System ; drug effects ; Saponins ; therapeutic use ; Triterpenes ; therapeutic use