The Protective Role of Interleukin-33 in Myocardial Ischemia and Reperfusion Is Associated with Decreased HMGB1 Expression and Up-Regulation of the P38 MAPK Signaling Pathway.

Interleukin-33 (IL-33) plays a protective role in myocardial ischemia and reperfusion (I/R) injury, but the underlying mechanism was not fully elucidated. The present study was designed to investigate whether IL-33 protects against myocardial I/R injury by regulating both P38 mitogen-activated-protein kinase (P38 MAPK), which is involved in one of the downstream signaling pathways of IL-33, and high mobility group box protein 1 (HMGB1), a late pro-inflammatory cytokine. Myocardial I/R injury increased the level of IL-33 and its induced receptor (sST) in myocardial tissue. Compared with the I/R group, the IL-33 group had significantly lower cardiac injury (lower serum creatine kinase (CK), lactate dehydrogenase (LDH), and cTnI levels and myocardial infarct size), a suppressed inflammatory response in myocardial tissue (lower expression of HMGB1, IL-6, TNF-α and INF-γ) and less myocardial apoptosis (much higher Bcl-2/Bax ratio and lower cleaved caspase-3 expression). Moreover, IL-33 activated the P38 MAPK signaling pathway (up-regulating P-P38 expression) in myocardial tissue, and SB230580 partially attenuated the anti-inflammatory and anti-apoptosis effects of IL-33. These findings indicated that IL-33 protects against myocardial I/R injury by inhibiting inflammatory responses and myocardial apoptosis, which may be associated with the HMGB1 and P38 MAPK signaling pathways.

Effects of Valsartan and Spironolactone on Growth Factors and Type Ⅰ Collagen in Aorta in Spontaneously Hypertensive Rat / 中国医师杂志

Objective To observe the effects of angiotensin Ⅱ(AngⅡ) AT 1 receptor antagonist,valsartan and mineralocorticoid receptor antagonist,spironolactone on growth factors and type Ⅰ collagen in aorta in spontaneously hypertensive rat(SHR).Methods Six-week male SHRs were divided into three groups at random:SHR control group,valsartan group and spironolactone group;six homogenous Wistar Kyoto(WKY) rats was served as normal control group.Valsartan 30mg?kg -1 ?d -1 ,spironolactone 20mg?kg -1 ?d -1 were respectively administered to rats in valsartan group and spironolactone group.Expressions of transforming growth factor ? 1(TGF ? 1),hepatocyte growth factor(HGF) and type Ⅰ collagen gene mRNA in aorta were determined by RT-PCR.Results Compared with those of untreated SHR group,levels of TGF?1 and type Ⅰ collagen gene mRNA expression in aortas treated with valsartan and spironolactone for 13 weeks were significantly reduced(P

Significance of ischemic ST-segment depression during supraventricular tachycardia in the detectation of coronary heart disease / 中国实用内科杂志

Objective To explore the significance of ischemic ST-segment depression during supraventricular tachycardia in the diagnosis of coronary heart disease(CAD).Methods From 1992 to 2008,65 patients with supraventricular tachycardia without clinical evidence of CAD in were divided into 2 groups:Group A included 48 cases with ischemic ST-segment depression during supraventricular tachycardia.Group B consisted of 17 cases with non-ischemic ST-segment depression.Group A was divide into 5 groups according to the age.They all underwent coronary angiography.Results 23(47.92%) of 48 cases in Group A had CAD,while none in Group B(P

The inhibiting effect of valsartan and spironolactone on cardiac fibrosis in spontaneously hypertensive rats / 中华老年医学杂志

Objective To explore the inhibiting effect of valsartan and spironolactone on cardiac fibrosis and the expression of integrin ? 1 and fibronectin in the heart of spontaneously hypertensive rats. Methods Eighteen 6 week old SHR were randomly divided into 3 groups with 6 in each: SHR control group, valsartan treating group(30 mg?kg -1 ?d -1 ) and spironolactone treating group ( 20 mg?kg -1 ?d -1 ). Six homogenous male WKY rats served as normal group. After 14 weeks of treatment, systolic blood pressure, left ventricular mass, the ratio of left ventricular mass to body weight (LVM/BW), collagen volume fraction(CVF) and perivascular collagen area(PVCA) were determined and compared among these groups. The expression of integrin ? 1 and fibronectin were also examined by immunohistochemical method. Results Compared with the untreated SHR S, systolic blood pressure was significantly decreased in both treatment groups. LVM/BW〔(2 84?0 14)?10 -3 vs(3 22?0 15)?10 -3 〕, CVF〔(3 21?0 22)%vs(4 00?0 28)%〕, PVCA〔(0 62?0 15)%vs(0 94?0 56)%〕 were lower in both treatment groups, these parameters in SHR V group were even lower than those in SHR S group. Compared with the untreated SHR S, the expression of integrin ? 1 was significantly reduced in SHR V group, while the expression of fibronectin was markedly reduced in both treatment groups. Conclusions Both valsartan and spironolactone could control blood pressure, and effectively inhibit the cardiac fibrosis. Valsartan could also inhibit the expression of cardiac integrin ? 1 and fibronectin, which might be the reason that valsartan is better than spironolactone in inhibiting cardiac fibrosis.

Effect of spironolactone and valsartan on expression of the active forms of mitogen-activated protein kinases in myocardium of spontaneously hypertensive rats / 第三军医大学学报

0.05),and that in valsartan group was higher than that in WKY group(P