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Tionship between neurons and astrocytes in HIV-associated dementia. J Neurovirol. 2012;19(2):123?0. 53. Kaul

by Shelly Fredericksen (2020-05-16)


Tionship between neurons and astrocytes in HIV-associated dementia. J Neurovirol. 2012;19(2):123?0. 53. Kaul M, Lipton SA. Mechanisms of neuronal injury and death in HIV-1 associated dementia. Curr HIV Res. 2006;4:307?8. 54. Bell DJ, Dockrell DH. Apoptosis in HIV-1 infection. J Eur Acad Dermatol Venereol. 2003;17(2):178?3. 55. Tardieu M, Hery C, Peudenier S, Boespflug O, Montagnier L. Human immunodeficiency virus type 1-infected monocytic cells can destroy human neural cells after cell-to-cell adhesion. Ann Neurol. 1992;32:11?. 56. Campbell GR, Loret EP. What does the structure-function relationship of the HIV-1 Tat protein teach us about developing an AIDS vaccine? Retrovirology. 2009;6:50. 57. Liu Y, Fusheng L, Qi Z, Hao Y, Hong K, Liu Y, et al. The effects of HIV-Tat DNA on regulating the immune response of HIV DNA vaccine in mice. Virol J. 2013;10:297.Submit your next manuscript to BioMed Central and take full advantage of:?Convenient online submission ?Thorough peer review ?No space constraints or color PK-11195 figure charges ?Immediate publication on acceptance ?Inclusion PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27309768 in PubMed, CAS, Scopus and Google Scholar ?Research which is freely available for redistributionSubmit your manuscript at www.biomedcentral.com/submit
Chang et al. Behav Brain Funct (2015) 11:28 DOI 10.1186/s12993-015-0074-RESEARCHOpen Access4-O--d-glucosyl-5-O-methylvisam minol, an active ingredient of Saposhnikovia divaricata, attenuates high-mobility group box 1 and subarachnoid hemorrhage-induced vasospasm in a rat modelChihZen Chang1,2,3*, ShuChuan Wu2, AijLie Kwan1,2 and ChihLung Lin1,Abstract Background: Highmobility group box 1 (HMGB1) was observed to be an important extracellular mediator involved in vascular inflammation associated with subarachnoid hemorrhage (SAH). This study is of interest to examine the effi cacy of 4Odglucosyl5Omethylvisamminol (4OGOMV), C22H28O10, on the alternation of cytokines and HMGB1 in an animal model. Methods: A rodent double hemorrhage SAH model was employed. Administration with 4OGOMV was initiated 1 h after animals were subjected to SAH. Basilar arteries (BAs) were harvested and cortexes examined for HMGB1 mRNA, protein expression (Western blot) and monocyte chemoattractant protein1 (MCP1) immunostaining. Cerebrospinal fluid samples were collected to examine IL1, IL6, IL8 and MCP1 (rtPCR). Results: Morphological findings revealed endothelial cell deformity, intravascular elastic lamina torture, and smooth muscle necrosis in the vessels of SAH groups. Correspondently, IL1, IL6 and MCP1 in the SAHonly and SAHplus vehicle groups was also elevated. 4OGOMV dosedependently reduced HMGB1 protein expression when compared with the SAH groups.(p < 0.01) Likewise, 400 g/kg 4OGOMV reduced IL1, MCP1 and HMGB1 mRNA levels as well as MCP1(+) monocytes when compared with the SAH groups.. Conclusion: 4OGOMV exerts its neuroprotective effect partly through the dual effect of inhibiting IL6 and MCP1 activation and also reduced PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27909987 HMGB1 protein, mRNA and MCP1(+) leukocytes translocation. This study lends credence to validating 4OGOMV as able to attenuate proinflammatory cytokine mRNA, lateonset inflammasome, and cellular basis in SAHinduced vasospasm. Keywords: 4Odglucosyl5Omethylvisamminol, Highmobility group box 1, Tumor necrotic factor, Subarachnoid hemorrhage, Vasospasm Background Subarachnoid hemorrhage (SAH)-induced cerebral vasospasm persists as a major cause of morbidity and mortality in patients suffering from aneurysm rupture [1?]. Owing*Corr.