Abstract
Objective: The present study aims to investigate the protective effect of methanol fraction of Morus alba (MEMA) leaves against hydrogen peroxide (H2O2)-induced U87MG cell toxicity and aluminum fluoride (ALF)-induced rat toxicity.
 Methods: The study was divided into in vitro and in vivo sections. U87MG cell lines were pre-treated with different fractions of MEMA for 20 h and further tested against 1000 ϻM of H2O2. The best fraction from in vitro studies was used to study the protective effects against ALF-induced neurotoxicity. Rats were divided i nto five different groups, and MEMA (200 and 400 mg/kg p.o) was administered for 14 days to the animals with α-tocopherol as the standard drug treatment. Behavioral studies were assessed using Barnes maze. The major biochemical measurements included catalase, superoxide dismutase and glutathione reductase, lipid peroxidation (LPO), and acetylcholinesterase (AchE) levels.
 Results: In vitro studies indicated MEMA as a potential candidate followed by AQMA and ethyl acetate. The MEMA fraction was able to ameliorate ALF-induced neurotoxicity in the behavioral assessment. The higher antioxidant content in the fraction decreased the LPO levels from 250±4.07 to 115±3.22 as well as elevated the levels of most of the endogenous antioxidant enzyme levels. AchE levels were also decreased to 33.89±0.71 from 38.94±0.64.
 Conclusion: Although the results obtained indicate that MEMA could significantly suppress oxidative stress-induced central neuronal damage both in vitro and in vivo, further mechanistic studies are required to delineate its neuroprotective pathway.
Highlights
Neurodegenerative diseases pose serious public health concerns with the most prevalent being Alzheimer’s disease (AD) followed by Parkinson’s disease (PD) [1]
The primary reactive oxygen species (ROS) scavenging system is associated with oxidative stress, and in the brain, the system constitutes of the antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GSH)
All fractions except PEMA reduced the cytotoxicity induced by H2O2, but pre-treatment with methanol fraction of Morus alba (MEMA) at 2.5 μg/ml significantly increased the cell viability compared to H2O2-treated cells and as well as the control (Table 1)
Summary
Neurodegenerative diseases pose serious public health concerns with the most prevalent being Alzheimer’s disease (AD) followed by Parkinson’s disease (PD) [1]. The evidence further suggests that AD will pose major neurological health concerns in the future [4]. Oxidative stress describes a state of imbalance in the production of free radicals and antioxidant defenses [8,9]. The primary reactive oxygen species (ROS) scavenging system is associated with oxidative stress, and in the brain, the system constitutes of the antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GSH). Any imbalance to this system could pave ways to amassing of ROS in the system and disrupt the normal poise required to protect the neurons from oxidative injury. One promising preventive or therapeutic measure for neuroprotection could be to suppress or attenuate the ROS production/accumulation through the exogenous supply of antioxidants and regain the disrupted endogenous oxidative balance [6]
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