ABSTRACT
Aim To investigate the effect of cotreat-ment norcantharidin (NCTD) and cisplatin (DDP) on the cisplatin sensitivity and proliferation in A549 cells, and whether YAP molecule involved in this process. Methods A549 cells were used as a model for inves-tigating the function of NCTD and DDP in this study. The expression of caspase-3,Annexin V,YAP,CTGF and Cyr61 were detected using RT-PCR and Western blot assay. The cell growth and proliferation were as-sessed by MTT and CCK-8 assay. Moreover, the tran-scriptional activity of YAP was detected by luciferase reporter gene assays. Results YAP was required for the cell growth and proliferation. NCTD,DDP and co-treatment of NCTD and DDP depressed cell viability, inhibited cell proliferation and promoted the sensitivity of cisplatin in A549 cells. Our results showed that the higher expressed oncogene YAP activated and promoted cell proliferation in lung cancer cells. Moreover, the high concentration of NCTD or DDP significantly re-duced cell proliferation, but cotreatment of NCTD and DDP in low concentration could significantly increase the cisplatin sensitivity via YAP pathway in A549 cells. Conclusions The cotreatment of NCTD and DDP in low concentration significantly reduces the transcriptional activity and protein level of YAP, then inhibits cell proliferation and thus increases the sensi-tivity of DDP in A549 cells.
ABSTRACT
Aim To investigate the effect of plumbagin on invasion and apoptosis of human hepatocellular car-cinoma ( HepG2 ) . Methods HepG2 cells were cul-tured in vitro with different concentrations of plumba-gin, then cell proliferation was observed by MTT as-say; cell invasion was observed by transwell invasion assay; cell apoptosis was detected by flow cytometry, and the protein expression of Bax, Bcl-2 was detected by immunocytochemistry. Results MTT results showed that plumbagin could significantly inhibit cell proliferation compared with the control group, and in a dose-dependent manner ( P ( P < 0. 01 ) . Flow cytometry showed that apoptosis rate was significantly higher in 4 , 8 μmol · L-1 group of plumbagin compared with that of the control group ( P<0. 01 ) . Immunocytochemistry showed that, with the increasing concentration of plumbagin, Bax protein expression increased, Bcl-2 protein expression was de-creased, both in a dose-dependent manner ( P <0. 01 ) . Conclusion Plumbagin can inhibit HepG2 cell proliferation and accelerate apoptosis of HepG2 cells, but also has the ability to inhibit HepG2 cell in-vasion.
ABSTRACT
Aim To investigate the effects of osthol on cell apoptosis and inflammatory cell infiltration after brain stab wound injury in mice. Methods The mice underwent the stab wound injury by a needle, then were randomly divided into sham operation group, model group, osthol 10, 20, 30 mg · kg-1 treatment group. The main examinations included mice brain wa-ter content; the apoptotic cytokines Bax, Bcl-2, Caspase-3 mRNA expression were assessed by PT-PCR; immunohistochemistry staining was used to de-tect neutrophils (MPO) and microglia (Iba-1) infiltra-tion and Caspase-3 positive cell expression around in-jured lesions. Results Treatment with osthole 20, 30 mg·kg-1 group significantly reduced the water content in injured brain, improved the ratio of Bax/Bcl-2, and reduced the expression of apoptosis cytokine Caspase-3 mRNA. Osthole 30 mg·kg-1 treatment group obvious-ly reduced the infiltration of neutrophils and microglial cells and significantly reduced the number of apoptotic cells around the injured cerebral cortex. Conclusion Osthole has therapeutic effect on stab wound injury in mice, and the possible mechanism may be by reducing the infiltration of inflammatory cells and reducing apop-totic cells.