Objective To investigate the changes and correlation between platelet activation and inflammatory response in patients with essential hypertension(EH). Methods Sixty-one patients with essential hypertension and sixty-four patients with paroxysmal supraventricular tachycardia as control group were enrolled in the study. The levels of high sensitivity C reactive protein ( hs-CRP ) and mean platelet volume ( MPV ) were measured and compared between the control group and the essential hypertension group. Results Compared with the control group,the levels of hs-CRP and MPV in the EH group were significantly higher( [3.51 ± 1.95]mg/L vs [ 1.15 ± 0. 77 ] mg/L, P ＜ 0. 05 ). The MPV in the EH group was significantly higher than that in the control group ( [ 11.29 ± 2. 18 ] flvs [ 9. 20 ± 2. 31 ] fl, P ＜ 0. 05 ). The level of hs-CRP positively correlated to the level of M PV (r = 0. 452, P = 0. 003 ). Conlusions There were inflammatory response and platelet activation in patients with EH and the serum levels of hs-CRP and MPV is correlated with the development of essential hypertension.

Objective To investigate the changes and clinical significance of serum prealbumin (PAB) and bilirubin in patients with coronary heart disease (CHD). Methods The levels of serum PAB and bilirubin were measured respectively in 234 patients with CHD (CHD group) and 77 patients with paroxysmal supraventricular tachycardia (PSVT, control group), and the former group was divided into stable angina pectoris (SAP) group with 80 patients,unstable angina pectoris (UAP) group with 84 patients and acute myocardial infarction (AMI) group with 70 patients,according to the chnical manifestation. Results The levels of total bilirubin (TBIL),direct bilirubin (DBIL) and indirect bilirubin (IBIL) in CHD group [ (11.8 ± 6.1 ), (4.8 ± 1.0) and (7.7 ± 2.7) μ mol/L] were significantly lower than those in control group [(14.6 ±5.6), (6.2 ±1.3) and (9.5 ±6.1)μmol/L] (P ＜0.05). The levels of TBIL, DBIL and IBIL decreased gradually from SAP group, UAP group to AMI group, but there was no significant difference among three groups (P ＞ 0.05 ). The levels of serum PAB in CHD group were also significantly lower than those in control group [(205.55 ±5.68) mg/L vs.(229.78 ± 9.62) mg/L] (P ＜ 0.05),and decreased gradually from SAP group,UAP group to AMI group [(215.73 ± 7.98), (214.12 ± 3.79) and (195.75 ± 7.07) mg/L],but there was no significant difference among three groups (P ＞ 0.05 ). Conclusion The levels of serum PAB and bilirubin are related to the severity of CHD, and can be used as important biochemical indicators in monitoring the attack and severity in patients with CHD.

Objective: To investigate the role of piperine on the transformation of endothelial cells into fibroblasts. Methods: Cultured human umbilical vein endothelial cells (HUVECs, 4-6 passage) were used for the main experiments. The transformation models of endothelial cells into fibroblasts were induced by transforming growth factor β (TGF-β) stimulation. HUVECs were divided into 6 groups: control group, TGF-β group and 4 groups treated with various concentrations of piperine (1, 5, 10, 20 μmol/L). CKK-8 was used to detect cell proliferation. The CD31/α-smooth muscle actin (α-SMA) expression level was detected by fluorescent staining. The vascular endothelial cadherin (VE-cadherin)/vimentin expression was detected by immunofluorescence staining. RT-PCR was used detect the mRNA expressions of transformation markers. Western blot was used to detect the protein expression of snail and twist. Results: TGF-β increased HUVECs proliferation (P<0.05), which could be significantly inhibited by 10 and 20 μmol/L of piperine, but not by 1 and 5 μmol/L of piperine. Immunofluorescence results demonstrated that TGF-β increased HUVECs transformation to fibroblasts as shown by downregulated expression of endothelial markers CD31, VE-cadherin, and upregulated expression of α-SMA and vimentin, again, these effects could be attenuated by 10 and 20 μmol/L piperine. The expression levels of collagen type Ⅰ and type Ⅲ were significantly higher in TGF-β group than in control group (P<0.05), significantly lower in TGF-β+10 μmol/L piperine group and TGF-β+20 μmol/L piperine group than in TGF-β group (P<0.05).In addition, RT-PCR results showed that TGF-β increased mRNA expression of transformation markers (snail1, snail2, twist1, twist2), while 10 and 20 μmol/L of piperine could significantly downregulated the mRNA expressions of these markers. The protein expression levels of snail and twist were significantly higher in TGF-β group than in control group (both P<0.05), which was significantly lower in TGF-β+20 μmol/L piperine group than in TGF-β group (both P<0.05). Conclusions Piperine can inhibit the transformation of endothelial cells into fibroblasts. This effect might be viewed as one of the potential mechanisms of reduced myocardial fibrosis post piperine treatment.