Search

Nodular lymphoid hyperplasia (NLH) in the small intestine is a rare benign lesion characterized by multiple small nodules on the intestinal surface. Patients with terminal ileal NLH may experience long-term abdominal pain, diarrhea, and abdominal distension, among other symptoms. Supplementation with probiotics could mitigate these symptoms. NLH is linked to the immune system, and it may result from accumulation of plasma-cell precursors due to a maturational defect during the development of B lymphocytes. The intestinal microbiome plays an essential role in the immune system. Thus, we speculate that the gut flora plays a key role in terminal ileal NLH.To explore the correlation between intestinal flora and terminal ileal NLH.We collected mucosal biopsy samples that were obtainedCompared with the control group, the terminal ileal NLH group showed an increased alpha diversity (Maintaining the microbial balance and supplementing targeted protective bacteria could improve symptoms and potentially reduce the risk of lymphoma transformation in patients with terminal ileal NLH.

To investigate the expression of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in human gastric cancer and it's mechanism in apoptosis and cell cycle arrest.Expression of 15-PGDH mRNA and protein was examined by immunohistochemistry, immunocytochemistry, reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting in tissue from human gastric cancer, gastric precancerous state (gastric polyps and atrophic gastritis), normal stomach, and gastric cancer cell lines. The relationship between gastric cancer, gastric precancerous state and 15-PGDH expression was determined. The association between expression of 15-PGDH and various clinicopathological parameters in gastric cancer was evaluated. Human gastric cancer cell line SGC-7901 was transfected with 15-PGDH expression plasmids. The effect of 15-PGDH on the cell cycle was examined by flow cytometry. The effect of 15-PGDH on apoptosis was examined by transmission electron microscopy, flow cytometry and transferase mediated nick end labeling (TUNEL) assay. Expression of cell cycle (p21, p27, p16 and p53) and apoptosis (Survivin, BCL-2, BCL-X(L), BAK and BAX) genes was analyzed by RT-PCR.Expression of 15-PGDH mRNA and protein in human gastric cancer tissues was significantly lower than in normal gastric tissues (P0.01). Expression in human gastric cancer cell lines MKN-28 and MKN-45 was reduced, and absent in SGC-7901 cells (P0.05). Reduction of 15-PGDH expression was also found in precancerous tissues, such as gastric polyps and atrophic gastritis (P0.01). There was a significant difference in expression of 15-PGDH among various gastric cancer pathological types (P0.05), with or without distant metastasis (P0.05) and different TNM stage (P0.01). Flow cytometry demonstrated a significant increase in apoptotic cells in SGC-7901 cells transfected with pcDNA3/15-PGDH plasmid for 24 h and 48 h (P0.01), and an increased fraction of sub-G1 phase after transfection (P0.05). TUNEL assay showed an increased apoptotic index in cells overexpressing 15-PGDH (P0.01). After transfection, expression of proapoptotic genes, such as BAK (P0.05), BAX and p53 (P0.01), was increased. Expression of antiapoptotic genes was decreased, such as Survivin, BCL-2 and BCL-X(L) (P0.01). Expression of cyclin-dependent kinase inhibitors p21 and p16 (P0.01) was significantly upregulated in cells overexpressing 15-PGDH.Reduction of 15-PGDH is associated with carcinogenesis and development of gastric carcinoma. 15-PGDH induces apoptosis and cell cycle arrest in SGC-7901 cells.

AIM: To investigate the effect and mechanism of action of erlotinib, an epidermal growth factor receptor (EGFR) small molecule tyrosine kinase inhibitor (TKI), in the human pancreatic cancer cell line BxPC-3 both in vitro and in vivo . METHODS: In vitro , human pancreatic cancer cell line BxPC-3 was exposed to varying concentrations of erlotinib, and its effects on proliferation, cell cycle distribution, apoptosis and the expression of proand antiapoptotic factors such as bcl-2, bcl-xl, bax and bak, and the expression of vascular endothelial cell growth factor (VEGF) were measured with 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometric analysis, terminal deoxynucleotidyl transferase-mediated nick end labeling assay (TUNEL), and reverse transcriptionpolymerase chain reaction (RT-PCR). Potential effect of erlotinib on angiogenesis was examined by tube formation assay. Tumor growth suppression was observed in xenografted nude mice with pancreatic cancer in vivo . Immunohistochemical (IHC) staining for EGFR and factor Ⅷ-related antigen was undertaken to detect the microvessel density and VEGF expression in tumor tissue in xenograft nude mice. RESULTS: Erlotinib, as a single agent, repressed BxPC-3 cell growth in a dose-dependent manner, triggered G1 arrest and induced cell apoptosis, and suppressed capillary formation of endothelium in vitro . Expressions of VEGF were significantly down-regulated at a high concentration of 200 μmol/L, however, the expressions of bcl-2 and bcl-xl were decreased at 50 μmol/L. In vivo , Erlotinib-treated mice demonstrated a reduced tumor volume, weight and microvessel density as compared to the control. IHC staining showed decreased expression of EGFR and RT-PCR had lower VEGF expression in treated mice. CONCLUSION: The in vitro and in vivo findings provide evidence that BxPC-3 cells are inhibited with erlotinib treatment. Inhibition of EGFR may be a promising adjuvant chemotherapy strategy in pancreatic cancer treatment.