Relations between fasting serum lipids and high-sensitivity C-reactive protein level in Chengdu residents / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the associations between fasting serum lipids and high-sensitivity C-reactive protein (hsCRP).</p><p><b>METHODS</b>Serum triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and hsCRP were measured in residents of Chengdu, China. Subjects with potential factors which might influence lipids and hsCRP were excluded, 580 subjects [mean age (62.3 ± 6.6) years; male: 58.7%] were finally recruited by random sampling methods.</p><p><b>RESULTS</b>There was a weak positive relationship between TG and hsCRP (r = 0.108, P = 0.01) and a weak negative relationship between HDL-C and hsCRP (r = -0.197, P < 0.001), this was also true in the sub-group with BMI < 24 kg/m(2) (r = 0.236, -0.140 respectively, all P < 0.001). In subjects with BMI < 24 kg/m(2), the hsCRP concentration was significantly higher in subjects with higher TG or lower HDL-C (all P < 0.05). hsCRP increased in proportion with the degree of dyslipidemia. After adjusting for gender, age, TC, LDL-C, fasting blood glucose, systolic blood pressure, diastolic blood pressure, history of hypertension and diabetes, smoking and alcohol drinking, logistic regression analysis showed that the odds ratio for increased hsCRP was 1.970 in subjects with either increased TG or lower HDL-C (P = 0.105) and 9.098 in subjects with both higher TG or lower HDL-C levels (P = 0.031). However, the observed relationship between TG, HDL-C and hsCRP in subjects with BMI < 24 kg/m(2) could not be observed in subjects with subjects with BMI > 24 kg/m(2) despite significant more cardiovascular risk factors in these subjects.</p><p><b>CONCLUSIONS</b>A weak positive correlation between TG and hsCRP as well as a weak negative correlation between HDL-C and hsCRP was evidenced in the whole cohort suggesting dyslipidemia might be related to enhanced inflammatory status. However, this relationship is not observed in subjects with BMI > 24 kg/m(2) despite existence of more cardiovascular risk factors in these subjects.</p>

Protective effects of shark hepatic stimulator substance against acute hepatic injury induced by acetaminophen in mice / 药学学报

<p><b>AIM</b>To investigate the protective effects of shark hepatic stimulator substance (sHSS) against acute hepatic injury induced by acetaminophen (AAP) in mice.</p><p><b>METHODS</b>Acute hepatic injury model of Balb/c mice was induced by a single intraperitoneal injection of AAP (200 mg.kg-1, i.p.). Serum ALT and AST activities were analyzed. The changes of microstructure and ultrastructure of hepatocyte were observed under optical and electronic microscope. The hepatocyte apoptosis was analyzed by flow cytometer and the expression level of Fas mRNA was determined by RT-PCR.</p><p><b>RESULTS</b>The activities of serum ALT and AST were significantly decreased and both necrosis and inflammatory infiltration were improved in the mice treated with sHSS 3.0 and 1.5 mg.kg-1. sHSS (3.0 mg.kg-1) prevented the ultrastructural changes of hepatocytes caused by AAP, decreased the percentage of apoptotic cells, and downregulated the expression level of Fas mRNA.</p><p><b>CONCLUSION</b>sHSS protected hepatocytes from AAP-induced injury, which might be associated with its protection of the mitochondria and inhibition of apoptosis and expression of Fas mRNA in hepatocytes.</p>