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Tavasoli S.,Tehran University of Medical Sciences | Zarnani A.H.,Avicenna Research Institute | Zarnani A.H.,Tehran University of Medical Sciences | Vafa M.,Tehran University of Medical Sciences | And 4 more authors.
International Journal of Preventive Medicine | Year: 2014

Background: Sepsis is one of the major causes of death in intensive care units. Oxidative stress and hyper-inflammation has been shown to be major cause of mortality and morbidity in septic cases. Pomegranate is a fruit considered for its antioxidant and anti-inflammatory properties. The aim of this study is to evaluate the effect of a standard pomegranate fruit liquid extract (POMx), on mortality and peritoneal bacterial load in cecal ligation and perforation (CLP) sepsis model. Methods: Male wistar rats were divided into four groups of 24 each: sham; CLP; prevention (consumed POMx [250 mg of polyphenols/ kg/day] for 4 weeks before CLP); treatment (received a single drink of POMx [250 mg of polyphenols/kg] after CLP). Each group was divided into three subgroups, each containing eight animals, for bacterial load and survival (with and without antibiotics) studies. Sepsis was induced by CLP surgery. Ten day survival rate was recorded. Peritoneal bacterial load was also assessed. Data were analyzed using Log-rank and Kruskal-Wallis tests. Results: There was no significant difference in survival rate of CLP, prevention and treatment groups, in subgroups without antibiotics. However, in subgroups with antibiotics, the prevention group had significantly lower survival rate than sham group (P < 0.05). Conversely, the bacterial load of prevention and treatment groups were significantly higher than sham group (P < 0.01). Conclusions: Our study demonstrates for the first time that pomegranate extract could increase mortality rate via increasing peritoneal cavity bacterial load, in CLP sepsis model. More studies to assess mechanisms of this effect are warranted. Source

Pazoki-Toroudi H.R.,Tehran University of Medical Sciences | Pazoki-Toroudi H.R.,Nano Vichar Pharmaceutical Ltd | Ajami M.,Tehran University of Medical Sciences | Habibey R.,Tehran University of Medical Sciences
Fundamental and Clinical Pharmacology | Year: 2010

Four pre-medication drugs are used to relieve pain, allay anxiety, reduce secretion and enhance hypnosis, were evaluated for their effects on ischemia reperfusion (I/R) injury which is one of the major complications of vascular and transplantation surgery. Right kidney was removed from female rats (210-250 g) 3 weeks before surgical procedure. Different doses of morphine (0.5, 2 and 5 mg/kg), promethazine (1, 2 and 5 mg/kg), atropine (0.1, 0.3 and 0.5 mg/kg) and alprazolam (0.08, 0.32 and 0.64 mg/kg) were administered subcutaneously 30 min before left renal artery occlusion and 6 h reperfusion. Left kidneys were processed for histological evaluations. Creatinine and BUN were measured in serum samples. Morphine, promethazine, atropine and alprazolam at all evaluated doses significantly decreased serum creatinine and BUN levels and histopathological scores. The effects of promethazine (1 mg/kg) and all doses of alprazolam were more potent than other pre-medication drugs and doses. This study suggested a protective effect of these pre-medication drugs on I/R injury. Although obvious studies are required, these findings may lead to effective therapies against I/R injury. © 2009 Société Française de Pharmacologie et de Thérapeutique. Source

Ajami M.,Shahid Beheshti University of Medical Sciences | Davoodi S.H.,Shahid Beheshti University of Medical Sciences | Davoodi S.H.,Comprehensive Cancer Control Center | Habibey R.,Tehran University of Medical Sciences | And 4 more authors.
Fundamental and Clinical Pharmacology | Year: 2013

Apoptosis, as well as necrosis, has an important role in post-ischemic renal pathology. The effect of pretreatment with Docosahexaenoic acid+Eicosapentaenoic acid (DHA+EPA) on renal injury and apoptotic protein expression was evaluated. Right nephrectomy was completed on male Wistar rats (255-300 g). The rats received DHA+EPA (200 mg/kg/day) of distilled water orally for 14 days before ischemia reperfusion (IR) or sham operation. A total of 81 rats were divided into three main groups with 6, 24 and 48 h of post-operation or reperfusion period. Serum creatinine (SCr), BUN, creatinine clearance (CCr) and fractional excretion of sodium (FENa) were measured. Tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activities, Bax and Bcl-2 protein expressions and renal histological injury were determined. SCr, BUN and FENa increased 6-48 h of reperfusion (P < 0.01). Tissue MDA content and Bax expression increased (P < 0.01) and CAT and SOD activities decreased (P < 0.05) in the IR group. DHA+EPA decreased SCr and BUN, FENa, tissue MDA levels (P < 0.05 vs. IR) and increased CAT and SOD activities and Bcl-2 expression (P < 0.05 vs. IR) for 6-48 h after ischemia. IR induced mild (6 h, P < 0.05) and severe (24-48 h, P < 0.01) tissue damage. Mild-to-moderate tissue damage was observed in DHA+EPA groups from 6 to 48 h of reperfusion period (P < 0.05 vs. IR, 24-48 h). In conclusion, the results suggest that pre-ischemic exposure to DHA+EPA could improve the outcome of early graft function by inhibition of IR-induced oxidative stress and apoptosis. © 2012 Société Française de Pharmacologie et de Thérapeutique. Source

Ajami M.,Tehran University of Medical Sciences | Eghtesadi S.,Tehran University of Medical Sciences | Razaz J.M.,Shahid Beheshti University of Medical Sciences | Kalantari N.,Shahid Beheshti University of Medical Sciences | And 6 more authors.
Neurological Sciences | Year: 2011

To determine the impact of ω3 fatty acids on post-ischemic expression of pro- and anti-apoptotic proteins in hippocampus, male rats were received 10 or 100 mg/kg [Docosahexaenoic acid (DHA) + Ecosapentaenoic acid (EPA); gavage; 21 days before ischemia to 2-10 days after ischemia]. Global cerebral ischemia reperfusion (IR) was performed using the four-vessel occlusion model; ischemia 8 min and reperfusion 6, 48 h and 10 days. IR increased Bcl-2 and Bax expression after 48 h (p < 0.05 and p < 0.01 vs. sham) and 10 days (only Bax; p < 0.05), without significant difference with DHA + EPA groups after 6 h. But after 48 h expression of Bcl-2 increased (p < 0.05 vs. IR) and Bax decreased (p < 0.05). At day 10 after ischemia expression of Bax in DHA + EPA acid groups was less than IR (p < 0.05) and in 100 mg/kg DHA + EPA group Bcl-2 expression was more than IR (p < 0.05). These data suggested that long-term gavage with DHA + EPA increase hippocampal neurons survival for days after ischemia, revealed by increased Bcl-2 and decreased Bax expressions. © 2011 Springer-Verlag. Source

Zare Mehrjerdi F.,Tehran University of Medical Sciences | Zare Mehrjerdi F.,University of Yazd | Aboutaleb N.,Tehran University of Medical Sciences | Habibey R.,Tehran University of Medical Sciences | And 8 more authors.
Brain Research | Year: 2013

Different signaling pathways are involved in tissue protection against ischemia reperfusion (IR) injury, among them mammalian target of rapamycin (mTOR) and related pathways have been examined in many recent studies. Present study evaluated the role of mTOR in remote ischemic preconditioning (RIPC) of hippocampus. Renal ischemia was induced (3 cycles of 5 min occlusion and 5 min reperfusion of unilateral renal artery) 24 h before global brain ischemia (20 min bilateral common carotid artery occlusion). Saline or rapamycin (mTOR inhibitor; 5 mg/kg, i.p.) was injected 30 min before RIPC. mTOR and phosphorylated mTOR (p-mTOR) expression, superoxide dismutase (SOD) activity and retention trial of passive avoidance test were determined 24 h after global ischemia. Apoptosis and neuronal cell density were assessed 72 h after hippocampal ischemia. RIPC decreased apoptosis (p<0.05 vs. IR), improved memory (p<0.05 vs. IR), and augmented p-mTOR expression and SOD activity after hippocampal ischemia (p<0.05 vs. IR). Rapamycin abolished all protective effects of RIPC (p<0.05 vs. RIPC+IR) suggesting a role for mTOR in RIPC induced hippocampal protection. © 2013 Elsevier B.V. All rights reserved. Source

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