The Protective Effect of Melissa officinalis L. in Visceral Hypersensitivity in Rat Using 2 Models of Acid-induced Colitis and Stress-induced Irritable Bowel Syndrome: A Possible Role of Nitric Oxide Pathway

BACKGROUND/AIMS: The aim of present study is to estimate the effects of Melissa officinalis L. (MO) on visceral hypersensitivity (VH), defecation pattern and biochemical factors in 2 experimental models of irritable bowel syndrome (IBS) and the possible role of nitric oxide. METHODS: Two individual models of IBS were induced in male Wistar-albino rats. In the acetic acid model, the animals were exposed to rectal distension and abdominal withdrawal reflex, and the defecation patterns were determined. In the restraint stress model, the levels of TNF-α, myeloperoxidase, lipid peroxidation, and antioxidant powers were determined in the (removed) colon. Rats had been treated with MO, L-NG-nitroarginine methyl ester (L-NAME), aminoguanidine (AG), MO + AG, or MO + L-NAME in the mentioned experimental models. RESULTS: Hypersensitive response to rectal distension and more stool defecation in control rats have been observed in comparison to shams. MO-300 significantly reduced VH and defecation frequency in comparison to controls. VH and defecation pattern did not show significant change in AG + MO and L-NAME + MO groups compared to controls. Also, significant reduction in TNF-α, myeloperoxidase, thiobarbituric acid reactive substances (TBARS), and an increase in antioxidant power in MO-300 group was recorded compared to controls. AG + MO and L-NAME + MO groups showed a reverse pattern compared to MO-300 group. CONCLUSIONS: MO can ameliorate IBS by modulating VH and defecation patterns. Antioxidant and anti-inflammatory properties along with its effect on the nitrergic pathway seem to play important roles in its pharmacological activity.

Protective Effect of selenium-based medicines on toxicity of three common organophosphorus compounds in human erythrocytes in vitro

Objective: Organophosphorus [OP] compounds are used to control pests, however they can reach the food chain and enter the human body causing serious health problems by means of acetylcholinesterase [AChE] inhibition and oxidative stress [OS]. Among the OPs, chlorpyrifos [CHP], malathion [MAL], and diazinon [DIA] are commonly used for commercial extermination purposes, in addition to veterinary practices, domestic, agriculture and public health applications. Two new recently registered medicines that contain selenium and other antioxidants, IMOD and angipars [ANG], have shown beneficial effects for OS related disorders. This study examines the effect of selenium-based medicines on toxicity of three common OP compounds in erythrocytes

Materials and Methods: In the present experimental study, we determined the efficacy of IMOD and ANG on OS induced by three mentioned OP pesticides in human erythrocytes in vitro. After dose-response studies, AChE, lipid peroxidation [LPO], total antioxidant power [TAP] and total thiol molecules [TTM] were measured in erythrocytes after exposure to OPs alone and in combined treatment with IMOD or ANG

Results: AChE activity, TAP and TTM reduced in erythrocytes exposed to CHP, MAL and DIA while they were restored in the presence of ANG and IMOD. ANG and IMOD reduced the OPs-induced elevation of LPO

Conclusion: The present study shows the positive effects of IMOD and ANG in reduction of OS and restoration of AChE inhibition induced by CHP, MAL and DIA in erythrocytes in vitro

On the protection by the combination of CeO[2] nanoparticles and sodium selenite on human lymphocytes against chlorpyrifos-induced apoptosis in vitro

Chlorpyrifos [CP] as an organophosphorus pesticide is thought to induce oxidative stress in human cells via producing reactive oxygen species [ROS] that leads to the presence of pathologic conditions due to apoptosis along with acetylcholinesterase [AChE] inhibition.This study aimed to evaluate the apoptotic effects of CP and to assess the protective potential of CeO[2] nanoparticle [CNP] and sodium selenite [SSe] by measuring cascades of apoptosis, oxidative stress, inflammation, and AChE inhibition in human isolated lymphocytes. In the present experimental study, we examined the anti-oxidative and AChE activating potential of CNP and SSe in CP-treated human lymphocytes. Therefore, the lymphocytes were isolated and exposed to CP, CP+CNP, CP+SSe, and CP+CNP+SSe after a three-day incubation. Then tumor necrosis factor-alpha [TNF-alpha] release, myeloperoxidase [MPO] activity, thiobarbituric acid-reactive substances [TBARS] levels as inflammatory/oxidative stress indices along with AChE activity were assessed. In addition, the apoptotic process was measured by flow cytometry. Results showed a significant reduction in the mortality rate, TNF-alpha, MPO activity, TBARS, and apoptosis rate in cells treated with CNP, SSe and their combination. Interestingly, both CNP and SSe were able to activate AChE which is inhibited by CP. The results supported the synergistic effect of CNP/SSe combination in the prevention of apoptosis along with oxidative stress and inflammatory cascade. CP induces apoptosis in isolated human lymphocytes via oxidative stress and inflammatory mediators. CP firstly produces ROS, which leads to membrane phospholipid damage. The beneficial effects of CNP and SSe in reduction of CP-induced apoptosis and restoring AChE inhibition relate to their anti-oxidative potentials

Propofol attenuates toxic oxidative stress by CCl4 in liver mitochondria and blood in rat

Anti-oxidant effects of propofol [2, 6-diisopropylphenol] were evaluated agains carbon tetrachloridet CCl[4] -induced oxidative stress in rat liver. 30 male rats were equally divided in to 6 groups [5 rats each]. Group I [control], while Group II was given CCl[4] [3 mL /Kg/day, IP]. Animals of Groups III received only propofol [10 mg/Kg/day, IP]. Group IV was given propofol+ CCl[4]. Group V was administered vitamin E [alpha-tocopherol acetate 15 mg/Kg/day, SC] .Animals of Group VII received alpha-tocopherol acetate + CCl[4] once daily for two weeks. After treatment, blood and liver mitochondria were isolated. Anti-oxidant enzymes activity such as glutathione peroxidase [GPx], superoxide dismutase [SOD] and oxidative stress marker such as reduced glutathione [GSH] and lipid peroxidation [LPO] concentration were measured. Oxidative stress induced with CCl[4] in liver mitochondria was evident by a significant increase in enzymatic activities of GPx, SOD, and LPO and decreased of GSH and vailability of mitochondria. Propofol and vitamin E restored CCl[4]-induced changes in GSH, GPx, SOD and LPO in blood and liver mitochondria. CCl[4] decreased viability of mitochondria that was recovered by propofol and vitamin E. It is concluded that oxidative damage is the mechanism of toxicity of CCl[4] in the mitochondria that can be recovered by propofol comparable to vitamin E