Combination therapy of the granulocyte colony stimulating factor and intravenous lipid emulsion protect the hippocampus after global ischemia in rat: focusing on CA1 region.

Brain stroke is one of the causes of human death and disability worldwide. Global ischemia results in the accumulation of free radicals in the neurons. It leads to histologically brain damage. The CA1 region of the hippocampus is a sensitive area for free radicals. This study investigated the combined therapy of the Granulocyte colony stimulating factor (G-CSF) and the Intravenous lipid emulsion (ILE). These neuroprotective agents play a role in the regeneration of neurons. They improve the learning ability and memory in rats induced global ischemia. We divided 35 rats into five groups. The groups were sham group, ischemia group, G-CSF group, ILE group, and G-CSF plus ILE group. Ischemia was induced by occlusion of the bilateral common carotid about 10 min. The drugs applied on days 1, 3 and 7. The treated groups received subcutaneous injection of 20 µg/kg G-CSF and intravenous injection of 5 ml/kg ILE. After two weeks, the memory and learning ability of the rats was evaluated by the shuttle box. Hematoxylin and Eosin and Nissl and TUNEL stainings were used to determine the necrosis, normal and apoptotic cells. The combined therapy increased normal cells compared to the ischemia group. They decreased the number of necrotic and apoptosis cells in other groups. The combined group improved the passive avoidance test compared to the other groups. The combination therapy of G-CSF plus ILE is more effective than each alone.

The Role of TNF-α in Aflatoxin B-1 Induced Hepatic Toxicity in Isolated Perfused Rat Liver Model.

Aflatoxin B-1 (AFB1) is one of the major mycotoxins causing food contamination. Previous studies have shown that AFB1 can induce carcinogenicity and toxic effects in the isolated perfused rat liver and these effects are associated with its metabolites and peroxidation activity. Here we surveyed whether these pathogenic effects of AFB1 are associated with TNF-α as an inflammatory cytokine in general liver damages. In this study, we used twenty male Wistar rats (250-300 g). Rats were divided into four groups. Control group was pre-treated with LPS and then perfused with KHBB. The second group was pretreated with PTX and LPS and then perfused with KHB. The third group was pre-treated with LPS and then perfused with AFB-1 and KHB. The last group was pretreated with LPS and PTX and then perfused with AFB1 and KHB. Results revealed that aflatoxin B1 significantly increased the enzyme activity of aminotransferase and levels of lipid peroxidation. Also, the levels of Glutathione decreased in the aflatoxin group significantly. TNF-α released in perfusate and increased in aflatoxin B1 group significantly and decreased in AFB-1+PTX. Exposure to Aflatoxin B1 may induce reactive oxygen species, so these species may induce overproduction of proinflammatory cytokines such as TNF-α and may cause more damage to hepatic cells.