Objective]The aim of this study was to investigate the level of serum C3,C4 and HDL-C in patients with coronary heart disease and the correlation between C3,C4 and HDL-C in patients with coronary heart disease.[Methods]We collected 251 cases of patient diagnosed with coronary artery disease by coronary angiography in Sun Yat-sen Memorial Hospital ,Sun Yat-Sen University from 2015-12 to 2016-07 and collected over our Boji Medical Center healthy people in 214 cases. These patients were divided into acute coronary syndrome group with 180 cases and stable coronary heart disease group with 71 cases. Each test results was adopted from clinical laboratory of Sun Yat-Sen Memorial Hospital ,Sun Yat-Sen University.[Results]Compared with the healthy control ,the difference of serum C3,C4 and HDL-C from acute coronary syndrome group and stable coronary heart disease group,was statistically significant(P<0.05). However,in patients with acute coronary syndrome and stable coronary artery disease groups,there was no significant correlation(P > 0.05)between C3,C4 and HDL-C. In healthy group,complement C3 negatively correlated with HDL-C,the difference was statistically significant(P<0.05).[Conclusions]In patients with coronary heart disease, the level of C3 and C4 increased,while the level of HDL-C decreased ,and inflammation may affect the relevance judgments between complement and HDL-C.

OBJECTIVE: To explore the effect of different Helicobacter pylori (H.pylori) clinical strains on the proliferation and apoptosis of gastric epithelial cells, and to observe the effect of H.pylori on gastric mucosa by Mongolian gerbil model infected H.pylori. METHODS: H.pylori isolates harvested from pathologically documented gastric carcinoma (GC, n=10) or chronic gastritis specimens (CG, n=10) were co-cultured with GES-1 cells individually. MTT assay and flow cytometry were used to determine the proliferation and apoptosis of GES-1 cells induced by H.pylori isolates. Mongolian gerbils were infected by the most (A strain) and the least (B strain) significantly proliferated H.pylori strains. Results When co-cultured with the cell/bacteria concentration ratio 1:1 and 1:50 for 12 h and the cell/bacteria concentration ratio 1:50 for 24 h, H.pylori clinical strains isolated from patients with gastric cancer promoted the proliferation of GES-1 cells, and there was significant difference in the absorbance compared with the group of gastritis strains(P<0.05). The apoptosis rate of the GC and CG groups increased significantly (P<0.05) compared with the control group when co-cultured with the cell/bacteria concentration ratio 1:50 and 1:200, and there was no significant difference between the GC group and the CG group (P>0.05). The incidences of intestinal metaplasia and dysplasia in the A strain group were significantly higher than those in the B strain group (P<0.05). CONCLUSION H.pylori strains from different disease sources have different effects on the proliferation of GES-1 cells. H.pylori isolated from gastric cancer can promote the proliferation of cells to different degrees and directly induce gastric precancerosis and gastric cancer.
Animals ; Apoptosis ; Cell Line ; Cell Proliferation ; Chronic Disease ; Gastric Mucosa ; cytology ; microbiology ; pathology ; Gastritis ; microbiology ; pathology ; Gerbillinae ; Helicobacter Infections ; pathology ; Helicobacter pylori ; pathogenicity ; Humans ; Metaplasia ; pathology ; Precancerous Conditions ; microbiology ; pathology ; Stomach Neoplasms ; microbiology ; pathology

OBJECTIVE: To construct the RNAi targeting tumor necrosis factor receptor associated factor (TRAF1) gene, and to explore the effect of interference targeting TRAF1 on the biological behavior of gastric cancer cells. METHODS: We detected the expression of TRAF1 in BGC823, SGC7901, and MGC803 gastric cancer cell lines through the real-time PCR and Western blot; then we constructed three pLVXshRNA- TRAF1-shRNAs expression vector targeting TRAF1. When TRAF1 was interfered successfully, we selected the strongest interference efficiency ShRNA by real-time PCR and Western blot. Based on interference targeting TRAF1 on gastric cancer, we tested the cell proliferation activity and apoptosis through MTT assay and flow cytometry, and the cell migration by transwell migration assay. RESULTS: The expression of TRAF1 was increased in BGC823, SGC7901, and MGC803 gastric cancer cell lines compared with gastric epithelial cells (P<0.05), and the highest expression was in BGC823 gastric cell line. In the three TRAF1 shRNAs, the strongest interference efficiency shRNA was pLVX-shRNA-TRAF1-shRNA2. When the gene TRAF1 of BGC823 was interfered, the cell growing power was weakened and the apoptosis rate increased, and the cell migration had no difference. CONCLUSION The expression of TRAF1 is up-regulated in gastric cancer cell lines BGC823, SGC7901, and MGC803, and the most obvious one is BGC823. The interference targeting TRAF1 can successfully inhibit the expression of TRAF1 in gastric cancer cell line BGC823. TRAF1 can inhibit the apoptosis of BGC823 cells.
Apoptosis ; genetics ; Base Sequence ; Cell Line, Tumor ; Humans ; Molecular Sequence Data ; RNA Interference ; RNA, Small Interfering ; genetics ; Stomach Neoplasms ; genetics ; metabolism ; pathology ; TNF Receptor-Associated Factor 1 ; genetics ; metabolism ; Transfection ; Up-Regulation ; genetics