Effect of xuezhlkang capsule in intervening different Chinese medical syndrome patterns of non-alcoholic fatty liver disease complicated with carotid atherosclerosis / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the intervening effects of Xuezhikang Capsule (XZK) on levels of blood lipid and other related indices in patients with different Chinese medical syndrome patterns of non-alcoholic fatty liver disease complicated carotid atherosclerosis (NAFLD-CAS), and to seek out the most appropriate pattern to indicate XZK for making guidance of its utilization.</p><p><b>METHODS</b>Chinese medical syndrome in 74 patients of NAFLD-CAS were classified into 4 patterns, 34 of Pi-deficiency phlegm-dampness pattern (A), 24 of dampness-heat accumulation pattern (B), 12 of phlegm-stasis intertwined pattern (C), and 4 of Gan-Shen yin-deficiency pattern (D). Excepting those of pattern D were excluded due to too small samples, all patients were treated with XZK for 3 months. Blood levels of blood lipids, including triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C), as well as high-sensitivity C-reactive protein (hs-CRP), and tumor necrosis factor alpha (TNF-alpha) were detected and compared before and after treatment.</p><p><b>RESULTS</b>The effective rate of XZK on patients of the three patterns, in A-C order, was 97.06%, 91.67%, 91.67%, respectively, with the optimal overall efficacy showed on pattern A. All the indices detected significantly decreased after treatment in all three patterns (P < 0.01), among them, excepting the difference of TG level between groups showed no significance (P > 0.05), the decrements of others were more significant in pattern A than in other two patterns (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>XZK could reduce the levels of blood lipids, hs-CRP and TNF-alpha in NAFLD-CAS patients, and the Pi-deficiency phlegm-dampness syndrome pattern was the optimal indication of XZK treatment.</p>

Effect of atorvastatin on advanced glycation end products induced monocyte chemoattractant protein-1 expression in cultured human endothelial cells / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of atorvastatin on advanced glycation end products (AGE) induced monocyte chemoattractant protein-1 (MCP-1) expression in human umbilical vein endothelial cells (HUVECs) and whether this effect could be linked to peroxisome proliferator-activated receptor-γ (PPAR-γ) and nuclear factor-κB (NF-κB).</p><p><b>METHODS</b>Grouping: (1) Blank control group; (2) BSA group; (3) AGE group: cells were incubated with different concentrations of AGE (10(-4), 10(-3), 10(-2) and 10(-1) g/L) for 24 hours; (4) AGE + Atorvastatin group: cells were incubated with different concentrations of atorvastatin (0.1, 1, 10 µmol/L) for 1 hour, then incubated with AGE (10(-1) g/L) for 24 hours; (5) PPAR-γ agonist (15 d-PGJ2) group: cells were incubated with 15 d-PGJ2 (10 µmol/L) for 1 hour, then incubated with AGE (10(-1) g/L) for 24 hours; (6) PPAR-γ inhibitor (GW9662) group: cells were incubated with GW9662 (5000 nmol/L) for 1 hour, then incubated with atorvastatin (1 µmol/L) and AGE (10(-1) g/L) for 24 hours. Collagenase was used to isolate the endothelial cell from human umbilical vein; RT-PCR was performed to examine the mRNA expression of MCP-1 and PPAR-γ; Western blot was performed to detect NF-κB p65 protein.</p><p><b>RESULTS</b>(1) The expression of MCP-1 mRNA was increased in proportion with increasing concentrations of AGEs which could be blocked by atorvastatin in a dose-dependent manner. (2) AGE (10(-1) g/L) significantly downregulated the expression of PPAR-γ mRNA (0.22 ± 0.08 vs. 0.69 ± 0.09, P < 0.01) while upregulated the expression of phospho-NF-κB p65 protein (0.78 ± 0.06 vs. 0.31 ± 0.01, P < 0.01) and nonphospho-NF-κB p65 protein (1.61 ± 0.16 vs. 0.59 ± 0.14, P < 0.01) compared with the control group which could be significantly attenuated by atorvastatin. (3) PPAR-γ agonist decreased the expression of phospho-NF-κB p65 protein (0.21 ± 0.01 vs. 0.78 ± 0.06, P < 0.01), nonphospho-NF-κB p65 protein (0.67 ± 0.14 vs. 1.61 ± 0.16, P < 0.01) and MCP-1 mRNA (0.17 ± 0.02 vs. 0.93 ± 0.12, P < 0.01) compared with AGE (10(-1) g/L) group. (4) PPAR-γ inhibitor antagonized the effect of atorvastatin on the expression of phospho-NF-κB p65 protein, nonphospho-NF-κB p65 protein and MCP-1 mRNA stimulated by AGE in HUVECs (P < 0.01).</p><p><b>CONCLUSION</b>The anti-inflammatory properties of atorvastatin in AGE stimulated HUVECs may partly be attributed to the effect on upregulation of PPAR-γ and downregulation of NF-κB signaling pathway.</p>