Mechanism of Xianglian Pills in improving dyslipidemia in obese mice induced by high-fat diet based on network pharmacology and intestinal flora / 中国中药杂志

The present study aimed to investigate the effect of Xianglian Pills(XLP) on lipid metabolism in obese mice and explore the underlying mechanism based on network pharmacology and intestinal flora. Firstly, network pharmacology was used to predict the possible effect of XLP on obesity. Secondly, an obese mouse model induced by a high-fat diet was established to observe changes in mouse body weight, adiposity index, liver and adipose tissue pathology. Lipid profiles, liver and kidney function markers, insulin content, and the expression of recombinant uncoupling protein 1(UCP-1) and PR structural domain protein 16(PRDM16) were measured. The 16S rRNA gene sequencing technology was used to analyze the changes in the intestinal flora. Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis showed that XLP mainly played a role in improving obesity by regulating lipolysis, type 2 diabetes mellitus, and insulin resistance. The results of animal experiments showed that XLP significantly reduced body weight, adiposity, blood lipid levels, and serum insulin levels in obese mice, while enhancing the expression of UCP-1 and PRDM16 in adipose tissue without causing damage to the liver or kidneys. The 16S rRNA gene sequencing results showed that XLP decreased the Firmicutes/Bacteroidetes(F/B) ratio at the phylum level, increased the relative abundance of Akkermansia and Bacteroides at the family and genus levels, and reduced the abundance of Allobaculum. Therefore, XLP can effectively improve lipid metabolism disorders in high-fat diet-induced obese mice, and the mechanism is related to the improvement of brown adipose function, the browning of white fat, the accelerated lipid metabolism, and the improvement of intestinal flora. However, its effect on promoting the conversion of white adipose to brown adipose still needs to be further studied.

Predictive Value of Lipoprotein-associated Phospholipase A2 in Patients With Acute Coronary Syndrome / 中国循环杂志

Objective: To explore the risk predictive value of lipoprotein-associated phospholipase A2 (Lp-PLA2) on acute coronary syndrome(ACS) and to study the relationship between Lp-PLA2 and the severity of coronary stenosis in ACS patients. Methods:A total of 155 ACS patients admitted in our hospital were enrolled. The patient were divided into 2 groups:AMI (acute myocardial infarction) group, n=49 and UA (unstable angina)group, n=106; in addition, there was a Control group, n=44 subjects with normal coronary angiography (CAG).Blood levels of Lp-PLA2 were examined, CAG was conducted and GRACE score, SYNTAX score,Gensini score were calculated. Based on Grace score, ACS patients were divided into 3 subgroups: Low risk subgroup, Grace score≤108, Mid risk subgroup,Grace score 109-140 and High risk subgroup,Grace score≥140.The above parameters were comparedamong different groups. Results: Compared with UA group and Control group, AMI group had increased blood level of Lp-PLA2, P<0.05. Compared with Low risk subgroup, High risk subgroup had much higher Lp-PLA2, P<0.05. Correlation analysis showed that Lp-PLA2 level was positively related to Gracescore (r=0.301, P<0.001). By SYNTAX score and Gensini score evaluation,Lp-PLA2 levels were similar among different subgroups. Conclusion:Blood level of Lp-PLA2 had certain risk predictive value in ACS patients; while it was not related to the severity of coronary stenosis.

Impact of NF-kappaB inhibitor on STAT3 translocation in PC-3 prostate cancer cell line / 中华男科学杂志

<p><b>OBJECTIVE</b>To observe the changes in the expressions of STAT3 and NF-KB in PC-3 cells after IL-6 stimulation and to verify the effects of the NF-KB inhibitor caffeic acid phenethyl ester (CAPE) on the expressions of p-STAT3 and IL-6 in the PC-3 prostate cancer cell line.</p><p><b>METHODS</b>PC-3 prostate cancer cells were treated with IL-6 at 20 ng/ml for 5, 10, 20, 30 and 45 min. The protein and mRNA expressions of STAT3 and NF-kappaB were measured by Western blot and real time PCR, respectively, and the cell cycle was detected by flow cytometry. The PC-3 cells were exposed to TNF-alpha or TNF-alpha + CAPE, followed by determination of the IL-6 expression in the supernatant of the cells by ELISA and the expression of p-STAT3 by Western blot.</p><p><b>RESULTS</b>After IL-6 stimulation, both the expression of p-STAT3 protein and the proliferation index of the PC-3 cells were significantly increased, and so were the expressions of IL-6 and p-STAT3 protein in the supernatant after TNF-alpha treatment (P < 0.05). TNF-alpha + CAPE induced statistically lower expressions of IL-6 and p-STAT3 than TNF-alpha alone (P < 0.05).</p><p><b>CONCLUSION</b>CAPE can inhibit IL-6 secretion induced by TNF-alpha in PC-3 cells and thus suppress STAT3 translocation. Therefore, by inhibiting the expression of NF-kappaB and affecting STAT3 and other related cell signaling pathways, CAPE may become a new therapeutic option for prostate cancer.</p>