The present study investigates the antioxidant and hepatoprotective effects of Capparis spinosa L. and Quercetin in tert-butyl hydroperoxide (t-BHP) induced acute liver damage. Different fractions of C. spinosa were examined for total phenolic content and antioxidant property. Among these fractions, hydroalcoholic extract was used to assess the hepatoprotective effect in tert-butyl hydroperoxide (t-BHP) induced hepatotoxicity model by determining serum biochemical markers, sleeping time and antioxidant assay such as reduced glutathione (GSH) as well as histopathological examination of liver tissues. The total phenolic and Quercetin contents of hydroalcoholic fraction were significantly higher than other fractions. It also showed high antioxidant activity. Pretreatment with hydroalcoholic fraction at the dose of 400 mg/kg and Quercetin at the dose of 20 mg/kg showed liver protection against t-BHP induced hepatic injury, as it was evident by a significant decrease in serum enzymes marker, sleeping time and MDA and an increase in the GSH, SOD and CAT activities confirmed by pathology tests. The final results ascertained the hepatoprotective and antioxidant effects of C. spinosa and Quercetin in a dose-dependent manner. Moreover, this study suggests that possible mechanism of this protection may be associated with its property of scavenging free radicals which may be due to the presence of phenolic compounds.
Cannabinoids, which are the active compounds of marijuana, produce some pharmacological effects similar to the opioids. In addition, there are functional interactions between the cannabinoid and opioid systems. In this study, we investigated the effects of intraperitoneal (i.p.) injection of opioid drugs on responses induced by intracentral amygdala (intra-CeA) microinjection of cannabinoid CB1 receptor agents in rats, using the elevated plus maze test of anxiety. I.p. injection of morphine (6 and 9 mg/kg) 30 min before testing, increased the percentage open arm time (%OAT) and the percentage open arm entries (%OAE), but not locomotor activity, showing an anxiolytic-like response. I.p. administration of the opioid receptor antagonist, naloxone (1 mg/kg) 15 min before testing, significantly reduced %OAT, but not %OAE and locomotor activity. The drug, however, tended to decrease locomotor activity. Intra-CeA administration of arachidonylcyclopropylamide (ACPA, an agonist shown to selectively activate CB1 receptors; 1.25 and 5 ng/rat) increased %OAT and %OAE but not locomotor activity, indicating an anxiolytic-like response. Coadministration of morphine (6 mg/kg, i.p.) plus ACPA (0.125 ng/rat, intra-CeA) increased the anxiolytic-like response. Administration of naloxone reversed the effects of intra-CeA injection of ACPA. Intra-CeA administration of the cannabinoid CB1 receptor antagonist, AM251 (2.5, 25, and 100 ng/rat) did not alter %OAT and %OAE, but the higher doses of the drug (25 and 100 ng/rat) reduced locomotor activity. Coadministration of morphine (6 mg/kg) or naloxone (0.1 mg/kg) with AM251 showed an anxiolytic-like response. In conclusion, the results may indicate an anxiolytic-like effect for cannabinoid CB1 receptors of the CeA and the existence of an interaction between the cannabinoid and the opioid systems in the modulation of anxiety.
Ahvaz, the capital city of Khuzestan Province, which produces Iran's most oil, is on the rolls of fame in view of air pollution. It has also suffered from dust storm during the recent two decades. So, emissions from transportation systems, steel, oil, black carbon, and other industries as anthropogenic sources and dust storm as a new phenomenon are two major concerns of air pollution in Ahvaz. Without any doubt, they can cause many serious problems for the environment and humans in this megacity. The main objective of the present study was to estimate the impact of ground-level ozone (GLO) as a secondary pollutant on human heath. Data of GLO in four monitoring stations were collected at the first step and they were processed and at the final step they were inserted to a health effect model. Findings showed that cumulative cases of cardiovascular and respiratory deaths which attributed to GLO were 43 and 173 persons, respectively. Corresponding RR for these two events were 1.008 (95% CI) and 1.004 (95% CI), respectively. Although we did not provide a distinction between winter and summer in case of mentioned mortalities attributed to GLO, ozone concentrations in winter due to more fuel consumption and sub adiabatic condition in tropospheric atmospherewere higher than those GLO in summer.
Cyclophosphamide (CP) is widely used in treatment of different cancers. Nephrotoxicity is one of the dose-limiting side effects of CP. This study was carried out to investigate the effect of melatonin (MEL) on CP-induced nephrotoxicity in mice. In this study, 50 Swiss albino mice (20-25 g) were randomly divided into five groups. Mice were pretreated with MEL intraperitoneally (i.p) in doses of 5, 10 and 20 mg/kg for five consecutive days, and CP (200 mg/kg, i.p) was administrated on the 5th day 1 h after the last dose of MEL. Then on day 6, blood samples were collected to determine serum creatinine (Cr) and blood urea nitrogen (BUN) levels. The kidneys were used for histological examination, biochemical assays and real-time PCR studies. Malondialdehyde (MDA), glutathione (GSH), protein carbonyl (PC), nitric oxide (NO) level, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and myeloperoxidase (MPO) activity were assessed in renal tissue. In addition, the expression of SOD2 and PGx1 was measured using real-time PCR method in renal tissue. Results showed that CP administration significantly increases Cr, BUN, MDA, PC, NO level and MPO activity. It also decreases renal GSH level, SOD, GPx and CAT activity. Pretreatment with MEL (especially 20 mg/kg, i.p.) for 5 days prevented these changes; however, it did not affect the SOD activity. Our results revealed that MEL might be useful for prevention of the nephrotoxicity induced by CP through ameliorative effects on biochemical indices and oxidative stress parameters.
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