[Association between matrix metalloproteinase-8 -799C/T polymorphism and instability of carotid plaque].

OBJECTIVE: To investigate the association between a -799C/T polymorphism in the promotor region of matrix metalloproteinase-8 (MMP-8) gene and instability of carotid plaque in Chinese Han population. METHODS: A total of 451 acute infarction patients from the Department of Neurology of Taizhou Hospital were divided into carotid vulnerable plaque group and carotid stable plaque group according to the results of carotid B-mode ultrasonography. Serum MMP -8 level was measured by the means of enzyme-linked immunosorbent assay (ELISA). At the same time, the MMP-8 -799C/T polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: Serum level of MMP-8 in the carotid vulnerable plaque group was higher than that in the carotid stable plaque group (t= 2.894, P= 0.004). The genotype distribution of -799C/T polymorphism between the two groups was significantly different (Chi-square = 13.65, P= 0.000). Serum level of MMP-8 in patients with TT genotype was higher than that in patients with CC genotype (t= 3.141, P= 0.001). CONCLUSION: The present study suggested that serum level of MMP-8 and the -799C/T polymorphism of MMP-8 gene are associated with carotid vulnerable plaque in Chinese Han population, and the T allele may be a predictor for the susceptibility of carotid vulnerable plaque.

[Observation of the promotion effect taurine on hepatic stellate cell's apoptosis in rat hepatic fibrosis model].

OBJECTIVE: To observe the effect of taurine on hepatic stellate cell's apoptosis induced by carbon tetrachloride (CCl4) in rats and to study its protective mechanisms. METHODS: CCl4-induced rat hepatic fibrosis was treated by taurine. Serum alanine aminotransferase (ALT), plasma protein, hyaluronic acid (HA), procollagen III (PC III), hepatic microsomal drug-metabolizing enzyme and anti-transforming growth factor beta1 (TGF-beta1) were determined. In addition, hepatic stellate cell's apoptosis and the pathological changes of liver tissue were observed under light microscope. RESULTS: The activity of serum ALT and the levels of serum HA, PC III were markedly reduced by taurine treatment. The hepatic cytochrome P450 (Cyt. P450) and cytochrome b5 (Cytb5) contents were increased by the same treatment. In addition, taurine could significantly inhibit the expression of TGF-beta1, promote the hepatic stellate cell's apoptosis, and relieve hepatic fibrosis. CONCLUSION: Taurine fulfills a role in promoting hepatic stellate cell's apoptosis in the case of hepatic fibrosis, it mitigates the liver injury, decreases the expression of TGF-beta1, and relieves hepatic fibrosis.

[The anticancer effect of artesunate and its mechanism].

AIM: To study the anticancer effect of artesunate and its mechanism. METHODS: To observe the effect of artesunate on the growth of solid tumor and the expression of PCNA, Bcl-2 and Bax genes in mice bearing H22 solid hepatic carcinoma. RESULTS: After administration of artesunate (ig, 300 mg.kg-1.d-1 x 7 d), growth of solid tumor was obviously inhibited, the tumor inhibitory rates were 49.1%, 48.7% and 46.6% and 46.6% in 3 experiments. The apoptosis of liver cancer cells were increased. Immunohistochemical staining showed that the number of Bcl-2 protein positive cells were decreased, but the number of Bax protein positive cells were increased. The PCNA positive cells were significantly lower than those in the control group. CONCLUSION: Artesunate showed obvious anticancer activity on H22 hepatic carcinoma bearing mice and undergo apoptosis of liver cancer cells. The mechanism of anticancer effect of artesunate may be related to down-regulation of the expression of PCNA and Bcl-2 genes and up-regulation of the expression of Bax gene.

Attenuation of portal hypertension by natural taurine in rats with liver cirrhosis.

AIM: To investigate the inhibitory effect of natural taurine (NTau) on portal hypertension (PHT) in rats with experimentally-induced liver cirrhosis (LC). METHODS: Experimentally-induced LC Wistar rats (20 rats/group) were treated with either oral saline or oral NTau for 6 consecutive weeks. Evaluation parameters included portal venous pressure (PVP), portal venous resistance (PVR), portal venous flow (PVF), splanchnic vascular resistance (SVR) and mean arterial pressure (MAP). Vasoactive substance levels including nitric oxide (NO), nitric oxide synthase (NOS) and cyclic guanosine monophosphate (cGMP) were also measured. Histological investigation of type I and III collagen (COL I and III) and transforming growth factor-beta(1) (TGF-beta1) was also performed. RESULTS: Treatment with NTau (1) significantly decreased PVP, PVR and PVF, and increased MAP and SVP; (2) markedly increased the vascular compliance and reduced the zero-stress of the portal vein; (3) markedly decreased the amount of NO and cGMP and activity of NOS; and (4) improved the pathological status of the liver tissue and reduced the expression of COL I, COL III and TGF-beta1. CONCLUSION: NTau inhibited the LC-induced PHT by improving hyperdynamic circulation, morphology of liver and biomechanical properties of the portal vein in experimentally-induced LC rats.