title: Potential contribution of oxidative stress and inflammation to anxiety and hypertension.
abstract: Previously, we have published that pharmacological induction of oxidative stress causes anxiety-like behavior in rats and also is associated with hypertension in these animals. Here, we report that sub-chronic induction of oxidative stress via pharmacological induction leads to i) reduction in glyoxalase (GLO)-1 and glutathione reductase (GSR)-1 expression; ii) calpain mediated reduction of brain derived neurotrophic factor (BDNF) levels; iii) NFκB mediated upregulation of proinflammatory factors interleukin (IL)-6 and tumor necrosis factor (TNF)-α and elevated angiotensin (AT)-1 receptor levels in hippocampus, amygdala and locus coeruleus regions of the brain. Acute oxidative stress has opposite effects. We speculate that regulation of GLO1, GSR1, BDNF, NFκB and AT-1 receptor may contribute to anxiety-like behavior and hypertension in rats.
authors.affiliation: Department of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, USA. ssalim@uh.edu
authors.forename: Samina
authors.initials: S
authors.lastname: Salim
authors.forename: Mohammad
authors.initials: M
authors.lastname: Asghar
authors.forename: Manish
authors.initials: M
authors.lastname: Taneja
authors.forename: Iiris
authors.initials: I
authors.lastname: Hovatta
authors.forename: Gaurav
authors.initials: G
authors.lastname: Chugh
authors.forename: Craig
authors.initials: C
authors.lastname: Vollert
authors.forename: Anthony
authors.initials: A
authors.lastname: Vu
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001007:Anxiety / Q000139:chemically induced / Q000473:pathology*; D001921:Brain / Q000378:metabolism*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D019328:Buthionine Sulfoximine / Q000009:adverse effects; D002154:Calpain / Q000378:metabolism; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D005980:Glutathione Reductase / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced / Q000473:pathology*; D007249:Inflammation / Q000150:complications*; D015850:Interleukin-6 / Q000378:metabolism; D007791:Lactoylglutathione Lyase / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019820:Xanthine / Q000009:adverse effects; D014969:Xanthine Oxidase / Q000009:adverse effects
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D015850:Interleukin-6; D044140:Receptor, Angiotensin, Type 1; D014409:Tumor Necrosis Factor-alpha; D019820:Xanthine; D019328:Buthionine Sulfoximine; D014969:Xanthine Oxidase; D005980:Glutathione Reductase; D002154:Calpain; D007791:Lactoylglutathione Lyase