Pterostilbene Attenuates Experimental Atherosclerosis through Restoring Catalase-Mediated Redox Balance in Vascular Smooth Muscle Cells.

Atherosclerosis, the major risk of cardiovascular events, is a chronic vascular inflammatory disease. Pterostilbene is a naturally occurring dimethylated analogue of resveratrol and has recently been demonstrated to be beneficial against cardiovascular diseases. However, the underlying mechanisms of pterostilbene on atherosclerosis remain elusive. Experimental atherosclerosis was induced by a high-fat diet (HFD) in apolipoprotein E knockout (ApoE-/-) mice. Pterostilbene was administered intragastrically for 16 weeks. We found that pterostilbene significantly attenuated thoracic and abdominal atherosclerotic plaque formation in HFD-fed ApoE-/-mice, accompanied by modulated lipid profiles and reduced production of proinflammatory cytokines (including IL-6, IFN-γ, and TNF-α). In addition, pterostilbene restored vascular redox balance in thoracic and abdominal aorta, evidenced by enhanced catalase (CAT) expression and activities, and decreased malondialdehyde and H2O2 production. Notably, pterostilbene specifically induced CAT expression and activities in the vascular smooth muscle cells (VSMCs) of thoracic and abdominal aorta. In vitro, pterostilbene markedly promoted the expression and activity of CAT and decreased ox-low-density lipoprotein (LDL)-mediated VSMC proliferation and intracellular H2O2 production, which was abolished by CAT siRNA knockdown or inhibition. Pterostilbene-induced CAT expression was associated with inhibition of Akt, PRAS40, and GSK-3ß signaling activation and upregulation of PTEN. Our data clearly demonstrated that pterostilbene exerted an antiatherosclerotic effect by inducing CAT and modulating the VSMC function.

Corrigendum: (-)-Epigallocatechin-3-Gallate Ameliorates Atherosclerosis and Modulates Hepatic Lipid Metabolic Gene Expression in Apolipoprotein E Knockout Mice: Involvement of TTC39B.

[This corrects the article on p. 195 in vol. 9, PMID: 29593532.].

(-)-Epigallocatechin-3-Gallate Ameliorates Atherosclerosis and Modulates Hepatic Lipid Metabolic Gene Expression in Apolipoprotein E Knockout Mice: Involvement of TTC39B.

Background: Aberrant chronic inflammation and excess accumulation of lipids play a pivotal role in the occurrence and progression of atherosclerosis. (-)-Epigallocatechin-3-gallate (EGCG), the major catechins in green tea, displayed anti-atherosclerotic properties in vivo and in vitro. However, the effects and underlying mechanism of EGCG on atherosclerosis remain unclear. Methods: Male apolipoprotein E-knockout (ApoE-/-) mice (7 weeks old) fed with high-fat diet (HFD) were treated with normal saline or EGCG (40 mg/kg/d, i.g.) for 18 weeks. Atherosclerotic plaque and liver lipid accumulation were measured by Oil Red staining. Plasma lipids and cytokines were detected using commercial kits. The expression of protein and mRNA was analyzed by western blot and quantitative real-time reverse transcription-polymerase chain reaction, respectively. Results: EGCG administration markedly attenuated atherosclerotic plaque formation in HFD-fed ApoE-/- mice, which were accompanied by increased plasma interleukin-10 (IL-10) level and decreased plasma IL-6 and tumor necrosis factor-α (TNF-α) levels. In addition, EGCG modulated high-fat-induced dyslipidemia, evidencing by decreased total cholesterol (TC) and low-density lipoprotein levels and increased high-density lipoprotein level. Meanwhile, EGCG treatment alleviated high-fat-mediated liver lipid accumulation and decreased liver TC and triglyceride. Mechanistically, EGCG significantly modulated high-fat-induced hepatic tetratricopeptide repeat domain protein 39B (TTC39B) expression and its related genes (Lxrß, Abcg5, Abcg8, Abca1, Srebf1, Scd1, Scd2, Fas, Elovl5, Mylip) expression in liver from ApoE-/- mice. Notably, EGCG remarkably induced hepatic liver X receptor α (LXRα) and LXRß expression and inhibited both precursor and mature sterol regulatory element binding transcription factor-1 (SREBP-1) expression. Conclusion: Taken together, our data for the first time suggested that TTC39B was involved in EGCG-mediated anti-atherosclerotic effects through modulation of LXR/SREBP-1 pathway.

[Effect of levosimendan on B-type natriuretic peptide levels in patients with advanced heart failure: a meta-analysis].

OBJECTIVE: To conduct a meta-analysis of the effect of levosimendan on B-type natriuretic peptide (BNP) levels and evaluate the therapeutic effect of levosimendan on advanced heart failure. METHODS: A meta-analysis was performed on the selected data to analyze the effect of levosimendan on BNP levels. RESULTS: Levosimendan decreased BNP by a mean of 337.66 [95%CI (-296.30, -379.02)] pg/ml 24 h after the administration, and by 259.92 [95%CI (-195.76, -324.08)] pg/ml at 48 h, and by 123.09 [95%CI(-53.32,-195.86)] pg/ml at 1 week. Levosimendan resulted in improvements of the cardiac function by about 29%, 22%, and 10% at 24 h, 48 h and 1 week after the administration. CONCLUSION: Levosimendan produces favorable effects on the cardiac functions and BNP levels.

[Remifentanil preconditioning lowers cardiac troponin I levels in patients undergoing off-pump coronary artery bypass graft surgery].

OBJECTIVE: To investigate the value of cardiac troponin I (cTnI) levels in assessing myocardial protection by remifentanil precondition against myocardial injury induced by off-pump coronary artery bypass (OPCAB). METHODS: Twenty-four patients undergoing OPCAB were randomized into control and remifentanil preconditioning group (n=12). All the patients received pretreatment with oral diazepam (10 mg), intramuscular morphine (10 mg) and hyosine (0.3 mg). General anesthesia was induced with midazolam (0.08 mg/kg), etomidate (0.1-0.3 mg/kg), fentanyl (5-10 microg/kg), and rocuronium (1 mg/kg), and maintained with isoflurane inhalation and propofol infusion. Intermittent fentanyl and pipecuronium were given intravenously. In remifentanil preconditioning group, remifentanil (5 microg/kg in 50 ml normal saline) was infused in 10 min after anesthesia induction, and only NS was administered in the control group. Blood samples were obtained before and at 0, 2, 6, 24, and 48 h after the operation to determine serum cTnI levels. RESULTS: In both of the two groups, the cTnI levels increased significantly at the postoperative time points (0, 2, 6, 24, and 48 h) as compared with those before the operation (P<0.05). The cTnI levels of remifentanil preconditioning group were markedly decreased after the operation in comparison with those of the control group (P<0.05). CONCLUSION: Remifentanil preconditioning decreases the cTnI levels and reduces myocardial injury induced by OPCAB.