Aim To determine the protective effect of NADPH oxidase against focal cerebral ischemia/reper-fusion ( I/R) injury in rats. Method A thread occlu-sion method was used to make a middle cerebral artery occlusion ( MCAO ) model. Apocynin ( 2. 5 mg · kg-1 ) was injected by tail vein 15 min before ischemi-a. Then, the neurological behavior, cerebral infarction volume, pathological morphological changes and the expression of Cx36, PKC, Bax, Bcl-2 of rats were de-tected after ischemia for 2 h, followed by reperfusion for 24 h. Results Compared with cerebral I/R group, administration of apocynin significantly reduced the neurological behavior scores and the cerebral in-farction volume percentage, alleviated the pathological morphological damage, increased the protein expres-sion of Cx36 and PKC, and reduced the Bax/Bcl-2 ra-tio of rats with focal cerebral I/R injury. Compared with apocynin group , apocynin combined with PKC inhibitor significantly reduced above protective effects. Conclusion Inhibition of NADPH oxidase could alle-viate cerebral I/R injury, increase the levels of Cx36, PKC proteins and reduce the Bax/Bcl-2 ratio.

OBJECTIVETo compare the biological behaviors of two drug-resistant testicular cancer cell lines established by different methods.

METHODSDrug-resistance was induced in testicular cancer cell lines exposure of the cells to increasing concentrations of or a high dose of cisplatin (I-10/DDPi and I-10/DDPh cell lines, respectively). The morphological characteristics of the two cell lines were observed microscopically. The resistance index of the cells was determined with MTT assay, and the cell growth curves were drawn. The cellular expression of resistance-associated proteins MDR1 and P-gp was detected by Western blotting. The cell invasion ability was assessed with Transwell assay.

RESULTSNormal testicular cancer cell line I-10 and the two resistant cell lines all showed an adherent growth pattern. Compared with I-10 cells, I-10/DDP cells exhibited slightly heterogenous cell sizes, irregular shapes, the presence of microvilli tentacles on the cell surface, and a scattered arrangement. The cisplatin resistance index of I-10/DDPi and I-10/DDPh cells were 3.924 and 3.099, respectively. Compared with I-10, the drug-resistant cell lines showed extended doubling time with increased expressions of MDR1 and P-gp and increased cell invasiveness, which was especially obvious in I-10/DDPi cells.

CONCLUSIONBoth increasing dose exposure and high-dose exposure to cisplatin can induce cisplatin resistance in testicular cancer cells, and the resistant cells established by the latter method better mimics clinical drug-resistant tumor cells.

ATP Binding Cassette Transporter, Sub-Family B ; metabolism ; Antineoplastic Agents ; pharmacology ; Cell Cycle ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; Cisplatin ; pharmacology ; Drug Resistance, Neoplasm ; Humans ; Male ; Neoplasms, Germ Cell and Embryonal ; pathology ; Testicular Neoplasms ; pathology

OBJECTIVETo investigate the protective effect of propofol against focal cerebral ischemia/reperfusion (I/R) injury in rats and its relation with gap junction.

METHODSSeventy adult male SD rats were randomly divided into sham-operated group, I/R group, low-, moderate-, and high-dose propofol groups (25, 50, 100 mg/kg; P25, P50, P100 groups, respectively), I/R+CBX group and P100+CBX group. Thread occlusion was used to induce middle cerebral artery occlusion (MCAO) in the mice for 2 h followed by reperfusion for 24 h. Longa's scores were used to evaluate the neurological behavior of the rats. TTC staining was used to measure the cerebral infarction volume and Western blotting was performed to detect the expressions of Cx43, PKC, Bax, and Bcl-2 in the brain of the rats.

RESULTSCompared with the I/R group, the rats pretreated with moderate and high doses of propofol showed significantly reduced neurological behavior scores and cerebral infarction volume percentage, and the effect was more obvious in high-dose propofol pretreatment group. CBX obviously enhanced the protective effect of propofol against I/R injury. Compared with those in the sham-operated group, the protein expression of Cx43 and the Bax/Bcl-2 ratio were increased and the protein expression of PKC was reduced in I/R group, and these changes were significantly reversed by high-dose propofol pretreatment; the effects of propofol were further enhanced by CBX.

CONCLUSIONThe protective effect of propofol against cerebral I/R injury may involve the inhibition of the gap junction via PKC signaling and by reducing the Bax/Bcl-2 ratio.

Animals ; Brain ; metabolism ; Brain Ischemia ; prevention & control ; Connexin 43 ; metabolism ; Gap Junctions ; Infarction, Middle Cerebral Artery ; Male ; Propofol ; pharmacology ; Protein Kinase C ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Signal Transduction ; bcl-2-Associated X Protein ; metabolism