Do NSAIDs inhibit growth of precancerous cervical cells in vitro?

BACKGROUND: Cervical cancer is one of the most common cancers worldwide. A promising, novel strategy for cancer treatment is chemoprevention. Non-steroidal anti-inflammatory drugs (NSAIDs) have chemopreventive effects on several cancers including those of cervix. There are few clinical trials of the effects of NSAIDs on precancerous cervical lesions but data from in vitro studies are lacking. OBJECTIVE: To study growth inhibitory effects of nonselective and selective NSAIDs on immortalized cervical cells in vitro. MATERIAL AND METHOD: Cytotoxicity of ibuprofen and celecoxib on immortalized cervical cells was analyzed by Cell Proliferation (MTT) Assay. Propidium Iodide (PI) Assay was used to analyze apoptotic cell death. RESULTS: Ibuprofen and celecoxib had significant growth inhibitory effects with IC50 of 3.00 +/- 0.44 mM and 30. 00 +/- 11.00 uM, respectively. Both drugs significantly induced apoptosis. CONCLUSION: Ibuprofen and celecoxib can inhibit growth and induce apoptotic cell death in immortalized cervical cells. results from the present study highlight the need for further in vivo researches and clinical trials in search of novel strategies for cervical cancer prevention.

Comparison of endothelial progenitor cell function in type 2 diabetes with good and poor glycemic control.

BACKGROUND: Endothelial progenitor cells (EPCs) play an important role in vascular repair and a decrease in the number of EPCs is observed in type 2 diabetes. However, there is no report on the change of EPCs after glycemic control. This study therefore aimed to investigate the EPC number and function in patients with good and poor glycemic control. METHODS: The number of EPCs was studied using flow cytometry by co-expression of CD34 and VEGFR2. The EPCs were cultured and characterized by the expression of UEA-I, CD34, VEGFR2, vWF and Dil-Ac-LDL engulfment, as well as the ability to form capillary-like structures. An in vitro study on the effect of hyperglycemia on the proliferation and viability of the cultured EPCs was also performed. RESULTS: The number of EPCs in type 2 diabetes was significantly decreased compared with healthy controls and there was an inverse correlation between the EPC numbers and plasma glucose, as well as HbA1C. The number and function of EPCs in patients with good glycemic control were recovered compared with those with poor glycemic control. When glucose was supplemented in the culture in vitro, there was a negative effect on the proliferation and viability of EPCs, in a dose-dependent manner, whereas the enhancement of apoptosis was observed. CONCLUSION: There was EPC dysfunction in type 2 diabetes which might be improved by strict glycemic control. However, the circulating EPC number and proliferative function in patients with good glycemic control did not reach the level in healthy controls.