Antioxidant Potential of Momordica Charantia in Ammonium Chloride-Induced Hyperammonemic Rats

The present study was aimed to investigate the antioxidant potential of Momordica charantia fruit extract (MCE) in ammonium chloride-induced (AC) hyperammonemic rats. Experimental hyperammonemia was induced in adult male Wistar rats (180–200 g) by intraperitoneal injections of ammonium chloride (100 mg kg−1 body weight) thrice a week. The effect of oral administration (thrice a week for 8 consecutive weeks) of MCE (300 mg kg−1 body weight) on blood ammonia, plasma urea, serum liver marker enzymes and oxidative stress biomarkers in normal and experimental animals was analyzed. Hyperammonemic rats showed a significant increase in the activities of thiobarbituric acid reactive substances, hydroperoxides and liver markers (alanine transaminase, aspartate transaminase and alkaline phosphatase), and the levels of glutathione peroxidase, superoxide dismutase, catalase and reduced glutathione were decreased in the liver and brain tissues. Treatment with MCE normalized the above-mentioned changes in hyperammonemic rats by reversing the oxidant-antioxidant imbalance during AC-induced hyperammonemia, and offered protection against hyperammonemia. Our results indicate that MCE exerting the antioxidant potentials and maintaining the cellular integrity of the liver tissue could offer protection against AC-induced hyperammonemia. However, the exact underlying mechanism is yet to be investigated, and examination of the efficacy of the active constituents of the M. charantia on hyperammonemia is desirable

Influences of Chronic Mild Stress Exposure on Motor, Non-Motor Impairments and Neurochemical Variables in Specific Brain Areas of MPTP/Probenecid Induced Neurotoxicity in Mice.

Parkinson's disease (PD) is regarded as a movement disorder mainly affecting the elderly population and occurs due to progressive loss of dopaminergic (DAergic) neurons in nigrostriatal pathway. Patients suffer from non-motor symptoms (NMS) such as depression, anxiety, fatigue and sleep disorders, which are not well focussed in PD research. Depression in PD is a predominant /complex symptom and its pathology lies exterior to the nigrostriatal system. The main aim of this study is to explore the causative or progressive effect of chronic mild stress (CMS), a paradigm developed as an animal model of depression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg. body wt.) with probenecid (250 mg/kg, s.c.) (MPTP/p) induced mice model of PD. After ten i.p. injections (once in 3.5 days for 5 weeks) of MPTP/p or exposure to CMS for 4 weeks, the behavioural (motor and non-motor) impairments, levels and expressions of dopamine (DA), serotonin (5-HT), DAergic markers such as tyrosine hydroxylase (TH), dopamine transporter (DAT), vesicular monoamine transporters-2 (VMAT 2) and α-synuclein in nigrostriatal (striatum (ST) and substantia nigra (SN)) and extra-nigrostriatal (hippocampus, cortex and cerebellum) tissues were analysed. Significantly decreased DA and 5-HT levels, TH, DAT and VMAT 2 expressions and increased motor deficits, anhedonia-like behaviour and α-synuclein expression were found in MPTP/p treated mice. Pre and/or post exposure of CMS to MPTP/p mice further enhanced the MPTP/p induced DA and 5-HT depletion, behaviour abnormalities and protein expressions. Our results could strongly confirm that the exposure of stress after MPTP/p injections worsens the symptoms and neurochemicals status of PD

Impact of stress on protein expression of DAT in striatum and SN of control and -MPTP/p treated mice.

<p>Protein expression of DAT (A) and quantified data (B) by densitometric analysis were shown. Values are expressed as arbitrary units and given as mean ± SD of three animals in each group. Values not sharing common alphabet differed significantly (P< 0.05) with each other.</p

Treatment schedule of the experimental study.

<p>Treatment schedule of the experimental study.</p

Impact of stress on protein expression of TH in cortex, hippocampus and cerebellum of control and -MPTP/p treated mice.

<p>Protein expression of TH (A) and quantified data (B) by densitometric analysis were shown. Values are expressed as arbitrary units and given as mean ± SD of three animals in each group. Values not sharing common alphabet differed significantly (P< 0.05) with each other.</p

Effect of stress on sucrose intake levels in control and MPTP/p treated mice.

<p>The level of sucrose intake was shown. Values are given as mean ± SD for six mice in each group. Values not sharing common alphabet differed significantly (P< 0.05) with each other.</p

Influence of stress on protein expression of DAT in cortex, hippocampus and cerebellum of control and MPTP/p treated mice.

<p>Protein expression of DAT (A) and quantified data (B) by densitometric analysis were shown. Values are expressed as arbitrary units and given as mean ± SD of three animals in each group. Values not sharing common alphabet differed significantly (P< 0.05) with each other.</p

Effect of stress on immunoreactivity of TH positive cells in control and MPTP/p treated mice.

<p>Immunoreactivity of TH positive cells (A) in SN and quantified data (B) were shown. Values are given as mean ± SD for three mice in each group. Values not sharing common alphabet differed significantly (P< 0.05) with each other.</p