ABSTRACT
Objective: To evaluate the effects of butylphthalide on microglia activation and inflammatory factors in frontal lobe of rats after chronic sleep deprivation. Methods: Rats were divided into four groups(nï¼8): control group, platform group, chronic sleep deprivation group and butylphthalide intervention group. Chronic sleep deprivation was performed in rats of chronic sleep deprivation group and butylphthalide intervention group for 18 h per day using the multiple platforms method, and sleep deprivation lasted for 28 days. At the same time, rats in platform group were put in platform, while rats in control group were in normal sleep. After 28 days of sleep deprivation, rats in butylphthalide intervention group were intraperitoneally injected with butylphthalide 100 mg/kg for 14 days, meanwhile rats in other groups were intraperitoneally injected with saline. Then brains were collected and ionized calcium binding adaptor molecule-1 (Iba-1) positive cells in cortex in frontal lobe were studied and counted. The expressions of inducible nitric oxide synthase (iNOS) and arginase1 (Arg1) in frontal lobe were detected by Western blot, and the mRNA levels of interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNF-α) were determined by real-time PCR. Results: Compared with control or platform group, the Iba-1 positive cells in chronic sleep deprivation group were large with long process, and increased cell counts were also found in the chronic sleep deprivation group (all Pï¼0. 05). Moreover, the mRNA expression levels of iNOS, IL-1, IL-6, TNF-α were increased, while the expression of Arg1 was decreased in frontal lobe in rats of the chronic sleep deprivation group compared with the control or platform group (all Pï¼0. 05). The Iba-1 positive cells in butylphthalide intervention group were reduced compared with chronic sleep deprivation group (Pï¼0. 05). And the mRNA expression levels of iNOS, IL-1, IL-6 and TNF-α were decreased, while the expression of Arg1 did not chang in rats of the butylphthalide intervention group compared with the chronic sleep deprivation group (all Pï¼0. 05). Conclusion: Butylphthalide might inhibit the activation and decrease the inflammatory factors in frontal lobe of rats after chronic sleep deprivation.
Subject(s)
Benzofurans/pharmacology , Frontal Lobe/drug effects , Microglia/cytology , Sleep Deprivation , Animals , Cytokines/metabolism , Microglia/drug effects , Nitric Oxide Synthase Type II/metabolism , RatsABSTRACT
OBJECTIVE: To evaluate the effects of prenatal radiation of 850ï½1 900 MHz mobile phone on white matter in cerebellum of adult rat offspring. METHODS: Pregnant rats were randomly divided into short term maternal radiation group, long term maternal radiation group and control group. Rats in short term and long term maternal radiation group were exposed to 6 h/d and 24 h/d mobile phone radiation during 1-17 days of pregnancy, respectively. The cerebellums of offspring rats at the age of 3 month(nï¼8)were taken. Cell morphology in cerebellum was studied by hematoxylin-eosin (HE) staining. The expressions of myelin basic protein (MBP), neurofilament-L (NF-L) and glial fibrillary acidic protein (GFAP) in cerebellum of rat offspring were detected by immunohistochemistry and Western blot. RESULTS: Compared to control group, the morphological changes of purkinje cells in cerebellum were obvious in rat offspring of short term and long term maternal radiation group. Compared to control group, decreased MBP and NF-L expressions and increased GFAP expression were observed in long term maternal radiation group(all Pï¼0.05). Compared to short term radiation group, the expressions of MBP and NF-L were down-regulated (all Pï¼0.05) and the expression of GFAP was up- regulated(Pï¼0.05) in long term radiation group. CONCLUSION: Prenatal mobile phone radiation might lead to the damage of myelin and axon with activity of astrocytes in cerebellum of male rat offspring, which is related to the extent of radiation.
Subject(s)
Cell Phone , Cerebellum/radiation effects , Electromagnetic Radiation , Prenatal Exposure Delayed Effects , White Matter/radiation effects , Animals , Cerebellum/pathology , Female , Glial Fibrillary Acidic Protein/metabolism , Male , Myelin Basic Protein/metabolism , Neurofilament Proteins/metabolism , Pregnancy , Random Allocation , Rats , White Matter/pathologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the pathogenesy deference between multiple and single site keloid by detecting gene mutation of Poly A site of transforming growth factor-beta1 receptor type II (TbetaR II).</p><p><b>METHODS</b>Collecting 20 keloid samples (6 multiple sites keloid samples and 14 single site keloid samples) and extracting DNA from them; designing and synthesizing the primers of Poly A site, then amplifying T1beta II DNA by PCR, analyzing the single strand conformation polymorphism about the products of PCR. After purifying the product of PCR, the site and type of the mutation rate of Poly A site was sequenced directly on the automatic sequencing equipment.</p><p><b>RESULTS</b>It had been found that the Poly A site of TbetaR II in keloid has deletion mutation, its mutation rate in multiple sites keloid was 50% (3/6), in single site keloid 7.1% (1/14). The mutation rate of Poly A site in multiple sites keloid was significant higher than that in single site keloid (P < 0.05)</p><p><b>CONCLUSION</b>It has been supposed that there are some deference in pathogenesy between the multiple and the single site keloid.</p>
