[Intraperitoneal chemotherapy for colorectal cancer peritoneal metastasis].

Peritoneal metastasis is one of the common site of colorectal cancer metastasis and associated with a poor prognosis. The core strategy for colorectal cancer peritoneal metastasis primarily revolves around a comprehensive treatment approach with cytoreductive surgery and systemic chemotherapy as the mainstay, supplemented by intraperitoneal chemotherapy. As an important supplement to treatment, intraperitoneal chemotherapy has broad application prospects. The main modalities are hyperthermic intraperitoneal chemotherapy (HIPEC), neoadjuvant intraperitoneal and systemic chemotherapy (NIPS), early postoperative intraperitoneal chemotherapy (EPIC), sequential postoperative intraperitoneal chemotherapy (SPIC), normothermic intraperitoneal chemotherapy (NIPEC) and pressurized intraperitoneal aerosol chemotherapy (PIPAC). To promote the standardized application of intraperitoneal chemotherapy, further research on the mechanisms underlying peritoneal metastasis of colorectal cancer, selection of effective intraperitoneal chemotherapy agents, determination of optimal timing and administration protocols, exploration of the feasibility of sequential intraperitoneal chemotherapy and conduction of valuable basic and clinical research are currently needed. This paper will review the development and origins of intraperitoneal chemotherapy, treatment modalities, as well as the current application status and prospects of various treatment approaches in the context of peritoneal metastasis of colorectal cancer.

[Galangin inhibits oxidized low-density lipoprotein-induced angiogenic activity in human aortic endothelial cells by downregulating lncRNA H19].

OBJECTIVE: To investigate the effects of galangin on angiogenic activity of oxidized low-density lipoprotein (ox-LDL)-induced human aortic endothelial cells (HAECs) and explore the underlying mechanisms. METHODS: HAECs incubated with 10, 20, 40, and 80 µmol/L galangin for 24 h were assessed for cell viability changes using MTT assay to determine the cytotoxicity of galangin. HAECs treated with 5 mg/mL ox-LDL and incubated with 20 and 40 µmol/L galangin for 24 h, and the cells overexpressing lncRNA H19 and incubated with 40 µmol/L galangin for 24 h were examined for lncRNA H19 level with qRT-PCR. The migration and tube formation capacity of the cells were observed using scratch assay and angiogenesis assay, and ROS levels in the cells were detected with flow cytometry. The protein expression levels of VEGFA, MMP-2 and MMP-9 in the treated cells were detected with Western blotting. RESULTS: Galangin at 10, 20, or 40 µmol/L produced no obvious toxicity (P>0.05), whereas 80 µmol/L galangin significantly inhibited the viability of HAECs (P<0.01). Treatment with ox-LDL significantly increased the expression of lncRNA H19 in HAECs. Galangin significantly lowered lncRNA H19 expression in ox-LDL-induced HAECs, suppressed cell migration, angiogenesis and ROS production level, and reduced the protein levels of VEGFA, MMP-2 and MMP-9 (P<0.01). The effects of galangin were blocked by overexpression of lncRNA H19 in the cardiomyocytes. CONCLUSION: The therapeutic effect of galangin for atherosclerosis is mediated by inhibiting lncRNA H19 expression to reduce ox-LDL-induced migration, oxidative stress, and angiogenesis of HAECs.