ABSTRACT
Vitamin C is a vital antioxidant that may antagonize the deleterious effects of smoking. While previous literature indicated the role of cigarette smoking in exacerbation of chronic renal and hepatic diseases, its impact on the healthy kidney and liver tissues needs to be elucidated. To evaluate the effects of administration of high dose of nicotine alone for three weeks or combined with vitamin C on the antioxidant defense status, functional, histological changes, and immunohistochemical demonstration of proliferating cell nuclear antigen [PCNA] expression in the liver and kidney tissues of the rat. Twenty four adult male albino rats were used. They were divided equally into four groups. Group I was the control group, Group II was given vitamin C only [300mg/kg i.p.], Group III was given nicotine only [5mg/kg i.p.] all were for 3 weeks. Group IV was given vitamin C for 3 days prior to nicotine injection then for 3 weeks with nicotine and for 2 days thereafter. Nicotine exposure caused significant reductions in the total body weight, relative liver and kidney weights, and significant elevations of oxidative stress marker; malondialdehyde in liver and kidney. In addition, in group III the levels of liver alanine transaminase, aspartate transaminase, and alkaline phosphatase were significantly increased compared to other groups. The liver and kidney of group III showed marked structural changes with epithelial shedding and cellular necrosis of parts of proximal and distal convoluted tubules, with partial loss of the brush border. The liver showed vacuolated hepatocytes cytoplasm, lipofuscin granules, peroxisomes, mitochondrial destruction, with dilated central vein and sinusoids. Dense PCNA immunostaining was detected in the liver and the kidney of group III Concomitant administration of vitamin C with nicotine revealed a noticeable amelioration of these structural and .functional changes. Vitamin C exerted a protective effect against nicotine-induced liver and kidney damage
ABSTRACT
This in vitro study aimed to investigate the possible mechanism underlying the protective effect of growth hormone [GH] on hippocampal function during periods of heightened glucocorticoid exposure. This study was conducted between January and June 2005 at the Joan C. Edwards School of Medicine, Marshall University, in Huntington, West Virginia, USA. The effects of the co-application of GH and corticosterone [CORT] were tested at different concentrations on the field excitatory postsynaptic potentials [fEPSPs] of the hippocampal slices of rats in two different age groups. Changes in the protein expression of N-methyl-D-aspartate receptor [NMDAR] subunits NR1, NR2B and NR2A were measured in hippocampal brain slices treated with either artificial cerebrospinal fluid [ACSF], low doses of CORT alone or both CORT and GH for three hours. The co-application of CORT and GH was found to have an additive effect on hippocampal synaptic transmission compared to either drug alone. Furthermore, the combined use of low concentrations of GH and CORT was found to have significantly higher effects on the enhancement of fEPSPs in older rats compared to young ones. Both GH and CORT enhanced the protein expression of the NR2A subunit. Simultaneous exposure to low concentrations of GH and CORT significantly enhanced NR2B expression and increased the NR2B:NR2A ratio. In contrast, perfusion with CORT alone caused significant suppression in the NR1 and NR2B protein expression and a decrease in the NR2B:NR2A ratio. These results suggest that NMDARs provide a potential target for mediating the GH potential protective effect against stress and age-related memory and cognitive impairment
ABSTRACT
Background: Tramadol is centrally acting analgesic that is frequently used clinically but its mechanism of action is still unclear
Aim of work: To evaluate tramadol analgesic activity, and its effect on gastric mucosa and hormones
Material and Methods: Thirty two adult male albino rats were used. Rats were divided into three groups: group [I] was injected with 3 doses of physiological saline [2ml kg[-1] every 12 h, i.p.], served as control; group [II] was injected with 3 doses of indomethacin [10 mg kg[-1] every 12 h, i.p.]; and group [III] was injected with 3 doses of tramadol [10 m kg[-1] every 12 h, i.p.]. 30 min after the first dose of injections, all groups were given 10 ml k[-1] of 1% acetic acid-saline i.p. to induce writhing. After 10 min following acetic acid injection, writhes numbers were counted over 20 min. Gastric mucosa was examined macroscopically and microscopically. Gastrin expression was detected by immunohistochemistry. Serum prostaglandin [PG], E2, ghrelin, and histamine concentrations were measured using ELISA kits
Results: Tramadol has lower analgesic effect compared to indomethacin. The gastric ulcer index was significantly lower in tramadol- versus indomethacin-treated group [P <0.0001]. Immunohistochemistry demonstrated higher gastrin immunoreactivity in indomethacin- and tramadol-treated groups versus control. Ghrelin serum levels were significantly suppressed by tramadol and indomethacin versus control that were coincident with gastric mucosal lesions. No significant changes in serum levels of PGE2 and histamine were obtained
Conclusion: Our results suggested that tramadol-induced gastric lesions are probably mediated by reduction of ghrelin and increase in gastrin expression. The antinociceptive and gastric effects of tramadol suggest that tramadol is relatively safe clinically in pain therapy