Ischemic postconditioning attenuates inflammation in rats following renal ischemia and reperfusion injury.

Ischemic postconditioning (IPoC) involves a series of brief rapid intermittent ischemic episodes applied at the onset of reperfusion in the previously ischemic tissue or organ. Previous studies have demonstrated that IPoC attenuates tissue damage induced by ischemia and reperfusion (I/R) injury. The aim of the present study was to investigate whether IPoC has a beneficial effect on inflammation in a rat model of renal I/R injury. Wistar rats were subjected to 45 min of ischemia followed by 24, 72 or 120 h of reperfusion (I/R group). In the IPoC group, rats subjected to I/R were treated with six cycles of 10 sec reperfusion followed by a 10-sec ischemic episode. Blood samples were collected for the determination of blood urea nitrogen (BUN) and creatinine (Cr) levels. Furthermore, histological examination and immunohistochemical staining for the localization of nuclear factor-κB (NF-κB) were performed. In addition, quantitative polymerase chain reaction (qPCR) analysis was used to determine the expression levels of intercellular adhesion molecule-1 (ICAM-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), while western blot analysis was used to detect the protein expression levels of NF-κB. The results indicated that the BUN and Cr levels increased significantly in the I/R group, while the IPoC rats showed evidently reduced renal damage. Immunohistochemical analysis revealed that the expression levels of NF-κB were decreased by IPoC. In addition, the qPCR results revealed that IPoC significantly inhibited the increased mRNA expression levels of ICAM-1, IL-6 and TNF-α, induced by I/R injury. Western blot analysis indicated that the expression levels of NF-κB were upregulated in the I/R group, while IPoC was shown to inhibit the expression. In conclusion, IPoC was demonstrated to exhibit potent anti-inflammatory properties against renal I/R injury.

Comprehensive analysis of temozolomide treatment for patients with glioma.

BACKGROUND: This analysis was conducted to evaluate the efficacy and safety of temozolomide based chemotherapy in treating patients with glioma. METHODS: Clinical studies evaluating the efficacy and safety of temozolomide based regimens for patients with glioma were identified using a predefined search strategy. Pooled response rates (RRs) were calculated. RESULTS: In temozolomide based regimens, 5 clinical studies including 152 patients with advanced glioma were considered eligible for inclusion. Four clinical studies included temozolomide. Systematic analysis suggested that, in all patients, pooled CR was 21% (32/152) , and PR was 21% (32/152). Grade 3/4 toxicity included neutropenia, thrombocytopenia, and anemia. No grade 3 or 4 renal or liver toxicity was observed. No treatment related death occurred with temozolomide based treatment. CONCLUSION: This systematic analysis suggests that temozolomide based regimens are associated with mild response rate and acceptable toxicity for treatment of glioma patients.

[Study on distribution of neural stem cells in the brain of Alzheimer disease transgenic mice through caudal vein transplantation].

OBJECTIVE: To observe whether neural stem cells (NSCs) can successfully permeate into the brain through the blood-brain barrier (BBB) of Alzheimer disease (AD) transgenic mice and explore the methods of distribution and migration. METHODS: NSCs were isolated from 12-day-old fetal mice, cultured, labeled with enhanced green fluorescent protein (eGFP) and then transplanted into 10 AD transgenic mice and normal mice as controls through caudal vein. The mice were killed 48 h, 1 w, 2 w, and 4 w after transplantation respectively. The brains of the mice were made into continual frozen sections, the distribution and migration of the eGFP-labeled NSCs were studied under fluorescence microscope. RESULTS: At different time points after transplantation the eGFP-labeled NSCs were diffusely distributed in the brain: distributed around the blood vessels in the first 48 h, and then migrated gradually towards the hippocampus and cortex until 4 weeks later. There were no obvious abnormal complications occurring after transplantation. CONCLUSION: NSCs can successfully permeate into the brain through the BBB of AD transgenic mice, and migrate into the brain parenchyma gradually.