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Heart failure is one of the two major problems in cardiovascular field in this century. Although the treatment of heart failure has made great progress, but the prognosis of heart failure is poor, Standardized drug treatment is still one of the most important and preferred methods for the treatment of heart failure. Heart failure is one of the serious vascular complications of diabetes, which affects the prognosis of diabetes. In recent years, studies have found that the new hypoglycemic drug sodium-glucose co-transporter 2 inhibitors can effectively reduce the risk of re-hospitalization and cardiovascular death in patients with or without diabetes, which has a landmark significance for the treatment of heart failure. This article will mainly discuss the latest mechanism of sodium glucose co-transporter 2 inhibitors in the treatment of heart failure.
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Emerging evidence has indicated that BRCC 36-mediated K63-linked ubiquitination modification was involved in diverse cellular functions , including endocytosis , apoptosis and DNA damage repair .We previously showed that activation of cGMP/PKG pathway con-tributed to the binding of BRCC36 and the pro-fibrotic factor Smad3.The current study tested the hypothesis that BRCC 36 functions as a negative regulator of transforming growth factor-beta ( TGF-β)/Smad3 pathway and participates in cardiac remodeling .In isolated adult mouse cardiac fibroblasts , we have demonstrated that TGF-β1 treatment significantly increased the expression of BRCC 36.Over-expression BRCC36 suppressed TGF-β1-induced Smad3 phosphorylation, nuclear translocation, extracellular matrix molecular expres-sion and cell proliferation .On the contrary, silencing BRCC36 by transfection of adenovirus-carrying BRCC36 shRNA potentiated to enhance the pro-fibrotic effect of TGF-β.In vivo, under chronic pressure overload condition-induced by transverse aortic constriction , myocardial pro-survival protein Bcl-2 and Mcl-1 expression were significantly decreased and the pro-apoptosis protein Puma was in-creased.However, the cardiac-specific over-expression of BRCC36 significantly increased myocardial Bcl-2 and Mcl-1 and inhibited Puma expression .Interestingly , we also found that sustained pressure overload resulted in a significant myocardial DNA injury in wild type mice, which was characterized by the increase of γH2AX level.However, cardiac-specific BRCC36 over-expression significantly decreased the level of γH2AX in the pressure overloaded heart in the transgenic mice , while effectively enhanced myocardial RAD 51 expression, a marker of DNA damage repair.Furthermore, BRCC36 over-expression effectively attenuated TAC-induced cardiac fibro-sis and remodeling in the transgenic mice , compared with the wild type mice .Collectively , the results have suggested that BRCC 36 ef-fectively protected heart against chronic pressure overload-induced cardiac remodeling though antagonizing TGF-β/Smad3 pathway and enhancing myocardial DNA injury repair response .
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Objective: To investigate the impact of thyroid hormone on atrial ifbrillation (AF) prevalence in patients with chronic heart failure (CHF). Methods: A total of 322 non-valvular heart disease CHF patients treated in our hospital from 2011-0-01 to 2012-10-01 were retrospectively studied. Based on previous history and the ECG at admission, the patients were divided into 2 groups: AF group,n=187 and Sinus rhythm group,n=135. The proifle of serum levels of free thyroxine (FT4), free triiodothyronine (FT3), hyroid stimulating hormone (TSH) and LDL-C were examined within 24 hours of admission; 12 lead ECG and echocardiography were conducted to analyze the related factor for AF occurrence. Results: Compared with Sinus rhythm group, AF group had increased FT4 level as 14.52 (12.74, 15.85) pmol/L vs 13.11 (11.68, 14.85) pmol/L,P Conclusion: High serum level of FT4 may increase the risk AF occurrence in CHF patients.
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The protein of BRCC36 is a kind of enzyme specifically hydrolyzing K 63-linked poly-ubiquitin chain and widely found in a variety of eukaryotic cells .BRCC36 recognizes diverse substrate proteins , and participates in various kinds of pathophysiological responses such as DNA damage repair , cell signal transduction and cell cycle control .It plays an important role in the process of cancer , angiogenesis and cardiac injury .This review discusses the progress in the inves-tigation on BRCC36 protein to provide the necessary information for searching new therapeutic targets of many diseases .
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Objective To explore the relationship between the plasma level of chemokines and clinical condition in patients with congestive heart failure (CHF). Methods The plasma levels of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) were measured in 62 patients with CHF (NYHA II～IV) and 18 healthy control subjects by ELISA and RIA, respectively. Results The levels of MCP-1 and IL-8 were significantly higher in CHF group than those in control group, and had a gradual increase along with the increasing of NYHA functional class. The increase of the chemokines levels was independent on the cause of the heart failure. The plasma MCP-1 level was significantly correlated with left ventricular ejection fraction, 6-minite walk distance, quality of life scores, and left ventricular end diastolic diameter, respectively(r=-0 422, -0 292, -0 421, 0 263, all P
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AIM:To explore the effects of pentoxifylline (PTX) on ventricular remodeling and cardiac function in dilated cardiomyopathy (DCM) rats.METHODS: Lewis rats were randomly allocated to a myocin-induced dilated cardiomyopathy (DCM) group receiving saline (n=10), a DCM group receiving PTX (PTX group; 25 mg?kg-1?d-1, ip, for 30 days, n=10) or healthy control group (n=10). The levels of tumor necrosis factor-? (TNF-?), interleukin-6 (IL-6) and IL-10 in the blood plasma were analyzed by ELISA. The extent of fibrosis was estimated using Masson's staining and immunohistochemistry analyses. Cardiac structure and function were measured by echocardiography.RESULTS: PTX decreased plasma levels of TNF-? and IL-6, and increased IL-10 level in DCM animals compared with DCM group [TNF-?: (7.21?0.24) ?g/L vs (19.30?1.31) ?g/L, P
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AIM: To investigate the roles of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) in delayed protection mechanism of anoxia preconditioning (APC) in rat cardiomyocytes.METHODS: The anoxia/reoxygention (A/R) injury, APC and PMA (an activator of PKC) preconditioning models were established in cultured neonatal rat cardiomyocytes and the effects of PKC and ERK blokers on the models were observed. ERK activity was assayed at 10 min after preconditioning in every group. The cellular MDA, SOD, cell viability and LDH release were measured at the end of the study. RESULTS: Compared with the cardiomyocyte in A/R group, the percentage of viable cells and SOD activity were greatly increased (P