Anti-Inflammatory and Anti-Oxidant Activity of Portulaca oleracea Extract on LPS-Induced Rat Lung Injury

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are classified as two lung complications arising from various conditions such as sepsis, trauma, and lung inflammation. Previous studies have shown that the extract of the leaves of Portulaca oleracea (PO) possesses anti-inflammatory and anti-oxidant activities. In the present study, the effects of PO (50⁻200 mg/kg) and dexamethasone (Dexa; 1.5 mg/kg) on lipopolysaccharide (LPS)-induced ALI were investigated. Subsequentially, the lung wet/dry ratio; white blood cells (WBC); levels of nitric oxide (NO); myeloperoxidase (MPO); malondialdehyde (MDA); thiol groups formation; super oxide dismutase (SOD) and catalase (CAT) activities; and levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, IL-10, prostaglandin E2 (PGE₂), and transforming growth factor (TGF)-β in the broncho alveolar lavage fluid (BALF) were evaluated in order to demonstrate the anti-oxidant and anti-inflammatory activity of PO. Our results show that PO suppresses lung inflammation by the reduction of IL-β, IL-6, TNF-α, PGE₂, and TGF-β, as well as by the increase of IL-10 levels. We also found that PO improves the level of WBC, MPO, and MDA, as well as thiol group formation and SOD and CAT activities, compared with the LPS group. The results of our investigation also show that PO significantly decreased the lung wet/dry ratio as an index of interstitial edema. Taken together, our findings reveal that PO extract dose-dependently displays anti-oxidant and anti-inflammatory activity against LPS-induced rat ALI, paving the way for rational use of PO as a protective agent against lung-related inflammatory disease

Yield of benzothiazine derivatives and catalysis by heteropolyacids

<p>An efficient heteropolyacid-catalyzed reaction for the synthesis of benzothiazine derivatives is reported. In this transformation, H₃PW₁₂O₄₀ was employed as a catalyst in a reaction involving 2-aminobenzenethiols, acetylenic esters, and malonate esters. Optimum conditions are developed in <i>i</i>-PrOH at 50˚C for 7 h.</p

Comparing The Effects of Selenium Nanoparticles and Selenium Nanocomposites on Food Intake and Anxiety-like Behaviors

Background & Objective: Selenium nanoparticles (Se -NPs) and selenium nanocomposites (Se -NCs) have different biological effects. Therefore, the present study aimed to compare the effects of selenium nanoparticles and selenium nanocomposites (Se –NCs) on anxiety, food intake, and brain histology of rats.  Materials & Methods: Thirty-two male adult Wistar rats were randomly and equally divided into four groups. The control group received saline, the Selenium powder group received 1 mg/kg /day selenium powder orally for 21 days, and the selenium nanoparticle group received three weeks of oral gavage of Se –NPs. The selenium nanocomposites group received three weeks of oral gavage of nanocomposites. Finally, cumulative food consumption and anxiety-like behaviors were assessed, and, after that, rats were bled and sacrificed for further biochemical and histopathological investigations. Results: Oral administration of Se powder at a dose of 1 mg/kg /day for 21 days had no significant effect on the brain superoxide dismutase (SOD), catalase (CAT) activities. There was also no significant change in the levels of brain glutathione concentration (GSH), brain MDA, and behavioral parameters. Selenium nanoparticles also showed no significant alterations in brain biochemical parameters, behavioral effects, and brain histology. The oral administration of Selenium nanocomposites significantly increased brain superoxide dismutase, catalase, and reduced glutathione content and had positive effects on behavioral parameters. Conclusion:  The present study showed that Se -NCs have behavioral effects and could induce significant biochemical changes in brain oxidative status

Protective Effect of Opuntia dillenii Haw Fruit against Lead Acetate-Induced Hepatotoxicity: In Vitro and In Vivo Studies

Lead is one of the most common environmental contaminants in the Earth’s crust, which induces a wide range of humans biochemical changes. Previous studies showed that Opuntia dillenii (OD) fruit possesses several antioxidant and anti-inflammatory properties. The present study evaluates OD fruit hydroalcoholic extract (OHAE) hepatoprotective effects against lead acetate- (Pb-) induced toxicity in both animal and cellular models. Male rats were grouped as follows: control, Pb (25 mg/kg/d i.p.), and groups 3 and 4 received OHAE at 100 and 200 mg/kg/d + Pb (25 mg/kg/d i.p.), for ten days of the experiment. Thereafter, we evaluated the levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), catalase (CAT) activity and malondialdehyde (MDA) in serum, and liver histopathology. Additionally, the cell study was also done using the HepG2 cell line for measuring the direct effects of the extract on cell viability, oxidative stress MDA, and glutathione (GSH) and inflammation tumor necrosis factor-α (TNF-α) following the Pb-induced cytotoxicity. Pb significantly increased the serum levels of ALT, AST, ALP, and MDA and liver histopathological scores but notably decreased CAT activity compared to the control group (p<0.001 for all cases). OHAE (100 and 200 mg/kg) significantly reduced the levels of serum liver enzyme activities and MDA as well as histopathological scores while it significantly increased CAT activity compared to the Pb group (p<0.001–0.05 for all cases). OHAE (20, 40, and 80 μg/ml) concentration dependently and significantly reduced the levels of MDA and TNF-α, while it increased the levels of GSH and cell viability in comparison to the Pb group (p<0.001–0.05 for all cases). These data suggest that OHAE may have hepatoprotective effects against Pb-induced liver toxicity both in vitro and in vivo by its antioxidant and anti-inflammatory activities

Protective Effects of N-Acetyl-L-cystein on 3,4-Methylene Dioxymethamphetamie-Induced Neurotoxicity in Cerebellum of Male Rats

Objective(s): 3-4, methylenedioxymethamphetamine (MDMA) causes apoptosis in nervous system and several studies suggest that oxidative stress contributes to MDMA-induced neurotoxicity. The aim of this study is to examine the effects of N-acetyl-L-Cystein (NAC) as an antioxidant on MDMA-induced apoptosis. Materials and Methods: 21 Sprague dawley male rats (200-250mg) were treated with MDMA (2×0,5mg/kg) or MDMA plus NAC (100mg/kg IP for 7 day). After last administration of MDMA, rats were killed, cerebellum was removed and Bax and Bcl-2 expression was assessed by western blotting method. Results: The results of this study showed that MDMA causes up-regulation of Bax and down-regulation of Bcl-2 and NAC administration attenuated MDMA-induced apoptosis. Conclusion: The present study suggests that NAC treatment may improve MDMA-induced neurotoxicity

Evaluation of Bcl-2 Family Gene Expression in Hippocampus of 3, 4-methylenedioxymethamphetamine Treated Rats

Objective: 3,4-methylenedioxymethamphetamine (MDMA) is an illicit, recreational drugthat causes cellular death and neurotoxicity. This study evaluates the effects of differentdoses of MDMA on the expression of apoptosis–related proteins and genes in the hippocampusof adult rats.Materials and Methods: In this expremental study,a total of 20 male Sprague Dawley rats(200-250 g ) were treated with MDMA (0, 5, 10, 20 mg/kg i.p. twice daily) for 7 days. Sevendays after the last administration of MDMA, the rats were killed. Bax and Bcl-2 genesin addition to protein expressions were detected by western blot and reverse transcriptionpolymerasechain reaction (RT-PCR).Results were analyzed using one-way ANOVA andp≤0.05 was considered statistically significant.Results: Our results showed that MDMA caused dose dependent up-regulation of Baxand down-regulation of Bcl-2 in the hippocampus. There was a significant alteration inbcl-2 and bax genes density.Conclusion: Changes in apoptosis-related proteins and respective genes relating to Baxand Bcl-2 might be involved in the molecular mechanism of MDMA-induced apoptosis