Moringa protects against nicotine-induced morphological and oxidative damage in the frontal cortex of Wistar rats

Project Abstract

<p>&nbsp;             <b>ABSTRACT&nbsp;</b></p><p>The use of nicotine-containing substances has been implicated in oxidative-induced neuronal damage in several neurological dysfunctions. This study assessed the antioxidant potentials of Moringa tea on the frontal cortex of Wistar rats. Twenty female Wistar rats were divided into 4 groups of 5 animals each. Group A (control) received normal saline, Group B received 5.71 mg/kg of Moringa tea, Group C was treated with 13.76 mg/kg nicotine, while Group D received 5.71 mg/kg of Moringa tea and 13.76 mg/kg nicotine, for 21 days. Homogenate of excised frontal cortex of rats obtained on day 22 was used to assess the level of malondialdehyde, catalase, superoxide dismutase and glutathione peroxidase. Histological sections were stained with heamatoxylin and eosin. Results showed increased activities of malondialdehyde and catalase in group C and a slight increase in group D compared with the control, while the activity of superoxide dismutase and glutathione peroxidase was reduced. The histological sections showed a normal architecture of the frontal cortex of rats treated with Moringa tea, but disrupted morphology in the group treated with Moringa tea and nicotineand further distortion in those that received nicotine only, when compared with the control group. These results suggest that Moringa tea may reduce the oxidative stress associated with nicotine consumption and limit the extent of structural damage in the frontal cortex of Wistar rats. Keywords frontal cortex; Moringa tea; nicotine; oxidative damage <br></p>

Project Overview

<p> Introduction&nbsp;</p><p>Nicotine is one of the principal components of tobacco; other constituents include many toxins and carcinogens such as tar, polycyclic aromatic hydrocarbon, heavy metals, carbon monoxide, arsenic and hydrogen cyanide that are linked to various diseases in the body.[1,2] The commonest source of nicotine is through cigarette smoking - the practice of burning tobacco and inhaling the smoke.[3] Nicotine replacement therapy (NRT) is used to decrease withdrawal symptoms triggered by smoking cessation in individuals who want to quit smoking and thus avoid the harmful effects of smoking and chewing tobacco.[4] Underlying the supposed connection between nicotine and cognitive enhancement is the role of nicotinic acetylcholine receptors (nAChRs) in attention, learning, memory, and cortical plasticity.[5] nAChRs normally bind endogenous neurotransmitter acetylcholine, but are also particularly responsive to nicotine. They are abundant in brain regions associated with learning and memory, including the frontal cortex,[6] and in primate and rodent models, depletion of acetylcholine in the prefrontal cortex results in impaired attentional performance.[5] Nicotine replacement products are most beneficial for heavy smokers who smoke more than 15 cigarettes per day. There are not adequate studies to show that NRT helps those who smoke fewer than 10 cigarettes per day.[7] Moringa oleifera commonly known as drumstick or horseradish tree,[8] is indigenous to the Northwestern part of India, but also widely distributed in the tropics, West Africa and Central America as well as the Caribbean.[9] Various parts of the tree have been used traditionally for the treatment of diabetes, rheumatism, hepatotoxicity, renal diseases and a variety of other diseases.[9–11] Given its therapeutic advantages, Moringa leaves have been processed into tea bags for easy consumption. The aim of the present study was to determine the effect of Moringa tea on oxidative stress markers and histoarchitecture of the frontal cortex following nicotine administration. <br></p><p> Materials and Methods&nbsp;</p><p>A total of 20 adult female Wistar rats with an average weight of 185±3.32 g were used for the study. Following the approval of the Ethics Committee of the University of Ilorin, the animals were housed in a wire gauzed cage in the animal house of the Faculty of Basic Medical Sciences at the University of Ilorin. The animals were allowed to acclimatize for two weeks prior to the commencement of the study. The animals were divided into four groups (A–D) of five animals each. Group A was orally treated with 1ml of distilled water, Group B was treated with 5.71 mg/kg body weight of Moringa tea, Group C was treated with 13.76 mg/kg nicotine in 0.1 ml of vehicle once daily as the maximum tolerated dose in an earlier study,[12] while Group D was treated with 5.71 mg/kg body weight of oral Moringa tea and 13.76 mg/kg nicotine i.p. once daily. All groups were treated for 21 consecutive days. Morinaga oleifera leaves were obtained and identified at the Department of Plant Biology of the University of Ilorin, Kwara State, Nigeria. Following weeks of sundrying, an aqueous extraction of the dry Moringa oleifera leaves was made and concentrated. Rats were weighed at 7-day intervals, beginning from day one of administration. 24 h after the final administration of Morinaga oleifera, animals for histology were euthanized using 20 mg/kg of ketaminei.p. andperfused transcardially with normal saline, followed by 4% paraformaldehyde (PFA). The brains were excised and post-fixed for 24 hin 4% PFA and processed manually for haematoxylin and eosin stain. Rats processed for enzymatic studies were sacrificed by cervical dislocation to eliminate the meddling of ketamine-induced change in biochemical status. The brains were excised following proper decapitation and dissection, and place in 30% sucrose solution. The frontal cortices of the right and left lobes of each animal were obtained and then homogenized manually with 30% sucrose solution. Each homogenate was centrifuged at 3000 rpm for 10 min and the supernatant was extracted for further enzymatic analysis. Enzymatic studies were carried out using the enzyme linked immunosorbent assay.&nbsp; The results obtained from enzymatic analysis were subjected to statistical analysis using the GraphPad Prism software, Version 6 (GraphPad Software Inc., San Diego, CA, USA). Malondialdehyde (MDA), glutathione peroxidase (GSH), catalase (CAT) and superoxide dismutase (SOD) results were plotted in one way ANOVA with Tukey’s multiple comparisons test. Data obtained were presented as mean ± standard error of mean, with determination of level of significance at p value less than 0.05. The outcomes were represented in bar charts with error bars to show the mean and standard error of mean, respectively. &nbsp;<br></p>