Journal of African Association of Physiological Sciences 2020-01-30T15:02:46+00:00 Anthony B. Ebeigbe (Professor) Open Journal Systems <p><em>Journal of African Association of Physiological Sciences</em> (J. Afr. Assoc. Physiol. Sci.)<strong> </strong>is an international, bi-annual official publication of African Association of Physiological Sciences. Both print and online forms are available. The journal is aimed at dissemination of information on diverse areas of research in Physiological Sciences disciplines and to showcase a representative cross-section of the kinds of research being carried out in Africa, in particular and globally. The journal was established in 2012 at the congress of African Association of Physiological Sciences held in Egypt. The journal will consider for publication, Full-length original research articles, short communications as well as review articles.</p><p>Other websites associated with this journal: <a title="" href="" target="_blank"></a></p><p><strong>J. Afr. Assoc. Physiol. Sci. </strong>applies the <a href="">Creative Commons Attribution (CC BY) license</a>, under which authors agree to make articles legally available for reuse, without permission or fees, for virtually any purpose. Anyone may copy, distribute or reuse these articles, as long as the author and original source are properly acknowledged.</p> Molecular mechanisms of aluminium neurotoxicity in animal models of Alzheimer’s disease 2020-01-30T15:02:37+00:00 M.S. Muhammad J.O. Ayo N.M. Danjuma A Abdulwahab A.S. Isa M.B. Maina <p>Alzheimer’s disease (AD) is the most common cause of dementia that affects one patient every seven seconds. With over 35 million people currently affected worldwide, it has been projected that the disease will affect about 115 million people by 2050. The disease is characterized by dysfunctional cellular and molecular networks and/or genomic and epigenomic interactions that affect the normal function of brain cells, leading to a defective cellular communication and function, and ultimately neurodegeneration. Aluminium (Al<sup>3+</sup>) is the third most abundant ubiquitous element in the earth crust which has gained easy access to humans and extensively used in daily life. It is an essential component of many materials used in households, such as clays, glasses, and alum. An increasing body of evidence implicates Al<sup>3+</sup> in the progression of events that lead to neurodegenerative diseases, some of which remains controversial, but it is widely accepted that Al<sup>3+</sup> is a recognised neurotoxin that could cause neurodegenerative diseases such as AD. The pathophysiological changes induced in Al<sup>3+</sup> neurotoxicity leading to AD result in critical impairments of the central nervous system functions, which are essential for healthy brain ageing. These changes include; axonal transport, neurotransmitter synthesis and synaptic transmission, disruption of calcium homeostasis, alteration of energy metabolism, phosphorylation/dephosphorylation of proteins, protein degradation, gene expression, formation of reactive oxygen species and inflammatory responses, inhibition of DNA repair system, activation of glial cells, reduction of activities of antioxidant enzymes, alterations of pathways of NF-kB and JNK, binding DNA, cell death, motor and cognitive decline. These multi-faceted pathways provide a link between Al neurotoxicity and AD by modulating both tau and amyloid beta hypotheses of AD.</p><p><strong>Keywords:</strong> Alzheimer’s disease, Aluminium chloride, Amyloid beta, Tau, Animal models</p> 2020-01-30T00:00:00+00:00 Copyright (c) Melatonin enhanced the restoration of biochemical profile in chlorambucil treated-rats: examination of after-withdrawal effects of the drug 2020-01-30T15:02:38+00:00 L.A. Olayaki W.J. Adeyemi E Adeyemi O Osawaru I Busura S Jimoh <p><strong>Background:</strong> In the wake of global prevalence of different types of cancer, the widespread use of chemotherapy poses threat to the integrity of the reproductive system. Although chlorambucil (Chrm) has anti-calcinogenic action, its administration has been associated with reproductive damage. Similar to chlorambucil, melatonin has anti-cancerous effect. Moreover, the hormone is claimed to protect the reproductive tissues from the insult of different disruptors of their functionality and histoarchitecture. Therefore, the present study investigated the effects of post-administration of melatonin in Chrm treated rats, with an interest in examining the after-withdrawal effects of the drug.</p><p><strong>Methods:</strong> Forty rats of ten animals per group were used for the study which lasted for six weeks. The control group received normal saline (vehicle; 0.1 ml/day, p.o.) for six weeks, while group 2 was administered saline for three weeks and then Chrm during the subsequent three weeks. However, in groups 3 and 4, Chrm was administered during the first three weeks; thereafter, they were administered saline and melatonin respectively during the subsequent three weeks. Chrm and melatonin were administered at 0.2 and 10 mg/kg b.w./day (p.o.) respectively.</p><p><strong>Results:</strong> The administration of Chrm significantly decreased gonadotrophin releasing hormone, follicle stimulating hormone, luteinising hormone, testosterone and antioxidant enzymes, but significantly elevated pro-oxidant and pro-inflammatory markers compared to the control group. Moreover, it was accompanied with selected significant alterations of semen parameters and lipid indices. However, restoration of baseline status of testosterone, catalase, total antioxidant capacity, malondialdehyde, lactate dehydrogenase, uric acid, sperm count, and free fatty acid was simply enhanced by the withdrawal of the drug, while that of gonadotrophin releasing hormone, testosterone, semen parameters, superoxide dismutase, catalase, c-reactive protein, lactate dehydrogenase, and high density lipoprotein cholesterol was facilitated by the administration of melatonin.</p><p><strong>Conclusion:</strong> The restoration of biochemical profile after chlorambucil treatment could be enhanced by the administration of melatonin.</p><p><strong>Keywords:</strong> chlorambucil; melatonin; reproduction; toxicity</p> 2020-01-30T00:00:00+00:00 Copyright (c) Lauric acid alleviates inflammation and structural changes in the lungs of type II diabetic male Wistar rats 2020-01-30T15:02:39+00:00 A.B. Dubo F.A. Dawud I.A. Umar E.A. Alex S Baiyekusi U Farra’u <p>Lauric acid is a medium-chain fatty acid that has been reported to possess anti-inflammatory, antioxidant and antibacterial properties. Diabetic complication in the lungs is characterized by infiltration of inflammatory mediators and structural alteration of the lung parenchyma. This study was designed to evaluate the effect of lauric acid on leucocytes infiltration in bronchoalveolar lavage fluid (BALF), concentration of tumor necrosis factor-α and lung histology of type II diabetic male Wistar rats. A total of thirty-five male Wistar rats were randomly divided into seven groups of five rats each as follows: Group I served as normal control; group II were normoglycemic rats, administered 125 mg/Kg bwt lauric acid. Group III served as diabetic control. Groups IV, V, VI and VII were diabetic Wistar rats treated with 125 mg/Kg bwt, 250 mg/Kg bwt, 500 mg/Kg bwt lauric acid and 100 mg/Kg bwt metformin respectively. The results obtained, showed a significant (P ≤ 0.05) increase in total white blood cell count and differential count of lymphocytes, neutrophils and macrophages in blood and BALF of the diabetic control compared to the normal control. However, there was a significant decrease in total and differential white blood cell count in blood and BALF of the diabetic groups treated with lauric acid compared to the diabetic control (P ≤ 0.05). The concentration of TNF-α was significantly higher in the lungs of diabetic rats compared to the normal control, but the concentration was significantly reduced after treatment with lauric acid (P ≤ 0.05). Lauric acid also reversed the reduced alveolar spaces in diabetic lungs. These results indicate that lauric acid reduced inflammation and reversed the histoarchitectural alterations in the lungs of type II diabetic male Wistar rats.</p><p><strong>Keywords:</strong> Lauric acid, Type II diabetes, Hyperglycemia, Lungs, Pneumopathy,<br />Leucocytes infiltration, Inflammation, Wistar rats</p> 2020-01-30T00:00:00+00:00 Copyright (c) Maternal serum progesterone levels and placental expression of progesterone receptors in insulin-resistant pregnant rats 2020-01-30T15:02:40+00:00 O.A. Ogunsola A.P. Arikawe B.O. Iranloye O.A. Adegoke <p><strong>Background:</strong> Maternal diabetes is known to impair placental function; however, its effect on placental expression of progesterone/oestrogen receptors and role of the placenta in foetal programming has not been well documented. The study assessed serum progesterone and oestradiol levels, placental morphology, placental progesterone and oestrogen receptors expression in insulin resistant rats.</p><p><strong>Methods:</strong> Virgin female rats were randomly divided into 2 groups; control group fed normal rat chow and insulin resistant group fed a diet containing 25% fructose w/w orally for 12 weeks. Rats in both groups were mated with proven male rats and presence of sperm cells in vaginal smear the following morning was taken as day 1 of pregnancy. Maternal blood and amniotic fluid samples were obtained and assessed for glucose, insulin, C-peptide, progesterone and oestradiol levels. Quantitative insulin sensitivity check index (QUICKI) was estimated from fasting blood glucose and insulin values. Placental tissues were isolated, weighed and fixed for morphological studies and the expression of oestrogen and progesterone receptors using immunohistochemical technique.</p><p><strong>Results:</strong> Maternal blood and amniotic fluid glucose, insulin, C-peptide levels, placental weight and diameter were significantly increased; while QUICKI was significantly lower (P &lt; 0.05) in the insulin resistant rats compared to control rats. Placental junctional zones were enlarged due to an increase in the number of glycogen and trophoblast giant cells in the insulin resistant rats. Progesterone receptor expression was down regulated, with no significant difference in oestrogen receptor expression in the insulin resistant rat placentae.</p><p><strong>Conclusion:</strong> The results suggest that maternal insulin resistance impairs progesterone production, placental morphology and down regulates placental progesterone receptor expression in this animal model of type 2 diabetes mellitus.</p><p><strong>Keywords:</strong> Insulin resistance, placenta receptors, progesterone, oestradiol, pregnancy</p> 2020-01-30T00:00:00+00:00 Copyright (c) Chronic exposure to high environmental temperature exacerbates sodium retention and worsens the severity of salt-induced hypertension in experimental rats via angiotensin receptor activation 2020-01-30T15:02:41+00:00 F.M. Agbaraolorunpo A.K. Oloyo C.N. Anigbogu O.A. Sofola <p><strong>Background:</strong> There is paucity of information on how exposure to high environmental temperature interacts with high dietary salt to influence cardiovascular outcome in the face of global warming.</p><p><strong>Method:</strong> This study investigated the impact of high environmental temperature (HET) on the cardio- renal indices of an animal model of hypertension (fed on high salt diet, HSD), and evaluated the effectiveness of angiotensin II receptor blocker (ARB), telmisartan, in modulating these indices. Fifty-six male Sprague Dawley rats (70-90g , 7 week old) were randomly assigned into seven groups of 8 rats, which include control rats (I), fed 0.3% NaCl diet; salt loaded rats (II), fed with 8% NaCl (high salt) diet; Heat rats (III), exposed to HET (37.5-38.5oC) 4 hours daily per week; salt loaded + Heat rats (IV), fed with 8% NaCl diet and exposed to HET daily. Next, salt loaded + ARB rats (V) , fed 8% NaCl diet and treated with telmisartan (30mg/kg); Heat +ARB rats, exposed to HET and treated with telmisartan (30mg/kg); salt loaded +HET+ARB rats (VI), fed with 8% NaCl diet, exposed to HET and treated with telmisartan (30mg/kg). Experiment lasted 8 weeks. Blood Pressure and heart rate were determined invasively and electrolytes by selective ion electrode method. Data analyzed using ANOVA, with P&lt;0.05 significant.</p><p><strong>Results:</strong> Systolic and Diastolic BP, Mean Arterial Pressure, Rate Pressures Product (RPP) (P&lt;0.05), and plasma Na+ (P&lt;0.05) were significantly higher with associated suppressed Na+ excretion (P&lt;0.05) in salt loaded rats exposed to HET compared to rats fed a high salt diet alone. Telmisartan significantly attenuated the elevated blood (P&lt;0.05) and RPP (P&lt;0.05), in the HSD rats exposed to HET, with no corresponding reduction in the rats fed a HSD alone.</p><p><strong>Conclusion:</strong> This indicates that chronic exposure to hot environment exaggerated cardiovascular response to high salt diet possibly via angiotensin II pathway with consequent enhanced ARB action.</p><p><strong>Keywords:</strong> Angiotensin II receptor; high salt diet; hot environment; environmental temperature; heat exposure; hypertension</p> 2020-01-30T00:00:00+00:00 Copyright (c) L-arginase induces vascular dysfunction in old spontaneously hypertensive rats 2020-01-30T15:02:42+00:00 O Arishe J McKenzie F Priviero A.B. Ebeigbe R Clinton Webb <p><strong>Background:</strong> Aging is a major non-modifiable risk factor for hypertension. Changes in aging are similar to those seen in hypertension in the vasculature. Also, aging increases the vascular dysfunction that occurs in hypertension. L-arginase action reduces substrate (L-arginine) availability for the formation of nitric oxide (NO). This reduces the level of NO and leads to reduced vasodilation and ultimately, vascular dysfunction. This study examines the hypothesis that age-dependent vascular dysfunction in SHRs is mediated by arginase.</p><p><strong>Methods:</strong> Young (12-14 weeks) and old (11-12 months) male Wistar and spontaneously hypertensive rats (SHR) were used. Mean arterial pressure (MAP) was measured in the rats. They were then euthanized and mesenteric resistance arteries (MRAs) and thoracic aortae were excised and placed in ice-cold physiological salt solution (PSS). Arterial segments were either snap-frozen in liquid nitrogen and stored for immunoblotting studies or cut into 2mm rings for reactivity studies. Cumulative concentration-response curves to acetylcholine (Ach; 10<sup>-9</sup> – 3x10<sup>-5</sup>M) and sodium nitroprusside (SNP; 10<sup>-12</sup> – 3x10<sup>-5</sup> M) were performed in the absence or presence (30-minute exposure) of L-arginase, 0.05U/ML (MRA) or 0.5U/ML (aorta). Vessels were pre-contracted with phenylephrine (PE; 3x10<sup>-6</sup>M)</p><p><strong>Results:</strong> MAP increased during aging in the SHRs p&lt;0.05 but not in the Wistar rats. Arginase impaired the endothelium-dependent relaxation responses of thoracic aortic and MRA arterial rings to Ach in the old Wistars and SHRs (Emax aorta: 29.42±2.19% vs 7.94±1.86%). Arginase also impaired endothelium-independent relaxation response to SNP in the old SHRs only (Emax aorta: 88.62±4.10% vs 31.45±10.61%). We also observed no differences in the serum arginase activity in the four groups of rats. On the contrary, arginase activity in the aortae of young Wistar rats was reduced compared to other groups.</p><p><strong>Conclusions:</strong> Arginase impairs both endothelium-dependent and –independent vasorelaxation responses, through the NO signaling pathway.</p><p><strong>Keywords:</strong> Hypertension, Arginase, aging, vascular dysfunction, endothelium, Nitric oxide</p> 2020-01-30T00:00:00+00:00 Copyright (c) Pattern of <i>Helicobacter pylori</i> infection in normal, overweight and obese adults in Nigeria 2020-01-30T15:02:43+00:00 F.L. Ciroma M.B. Akor-Dewu M.A. Kana J.O. Ayo A Mohammed <p><strong>Background:</strong> Obesity is a state of chronic energy imbalance which has a multifactorial origin, but mainly believed to be due to overeating and underactivity. Prevalence of obesity is rising to an epidemic level world-wide. Obesity is associated with metabolic and cardiovascular complications, and recently, <em>Helicobacter pylori</em> infection (<em>H. pylori</em>).<em> H. pylori</em> is a gram-negative bacteria that colonizes the gastric mucosa, and is highly prevalent. It has been implicated in the pathogenesis of chronic gastritis, gastric cancer and inflammation. Previous studies observed <em>H. pylori</em> infection as a risk factor to development of obesity, but other reports suggest a protective role of <em>H. pylori</em> against obesity. There is inconsistent data across various population studies.</p><p><strong>Aim:</strong> To investigate the pattern of <em>H. pylori</em> in overweight and obese subjects in Nigeria.</p><p><strong>Methods:</strong> A total of 277 subjects (185 males and 92 females), within the age of 18- 72 years were recruited from a university in northern part of Nigeria. Anthropometric and blood pressure were measured, and participants were grouped into normal, overweight and obese. <em>H. pylori</em> was serologically assayed by ELISA.</p><p><strong>Results:</strong> A total of 149 (53.8%) subjects were within normal body mass index (BMI), 55 (19.9%) were overweight and 73 (26.4%) were obese. From a total of 125 respondents who were positive to <em>H. pylori</em>, 52% were within normal group, 19.2% were overweight, and 28.8% were obese.<em> H. pylori</em> infection was present in 64/185 (34.6%) of males and 61/92 (66.3%) of females in the studied population. Out of obese respondents, only 16% of obese males were positive to <em>H. pylori</em>, but up to 43% of obese females were <em>H. pylori</em> positive.</p><p><strong>Conclusion:</strong> In the present study, <em>H. pylori</em> infection was less in obese males and more in the normal group. In the females, <em>H. pylori</em> was more in the obese and less in normal and overweight groups.</p><p><strong>Keywords:</strong> <em>Helicobacter pylori</em>, Overweight, Obese, Male, Females; Nigeria</p> 2020-01-30T00:00:00+00:00 Copyright (c) The effects of <i>Jatropha tanjorensis</i> aqueous leaf extract on haematological parameters in Wistar rats 2020-01-30T15:02:44+00:00 A.M. Danborno F Tarfa J.E. Toryila E.U. Awheela V.T. Shekarau <p>Immense benefits have been derived by man from using medicinal herbs in treatment and management of disease because they are relatively safer, more affordable and sometimes offer better therapeutic value than synthetic drugs. The leaves of <em>Jatropha tanjorensis</em> have been used for the treatment of diabetes mellitus. This study investigated the Haematological indices of aqueous leaf extract of <em>Jatropha tanjorensis</em> in male Wistar rats.25 male Wistar rats weighing 150-180g were used for the research. The rats were divided into five groups of five rats each. Group I served as control, and groups II, III, IV and V were administered 125mg, 250mg, 500mg, and 750mg per kilogram body weight respectively of the<em> Jatropha tanjorensis</em> leaf extract daily for 14 days. The rats were maintained under standard laboratory conditions at the animal house in the Faculty of Basic Medical Sciences, Bingham University, Nasarawa State The rats were sacrificed by cervical dislocation and blood collected by cardiac puncture. 2mls of blood were placed in EDTA bottle for the determination of haematological parameters using Auto Haematology Analyzer. The result shows significant increase in RBC, Hb, PCV, WBC, and PLT in the groups treated with 125mg/kg ,250 mg/kg and 500mg/kg aqueous leaf extract of <em>Jatropha tanjorensis</em> when compared with the control(P&lt;0.05). However, at higher dose of 750mg/kg of aqueous leaf extract of <em>Jatropha tanjorensis</em>, there was a decrease in RBC, Hb, PCV, WBC, and PLT (P&lt;0.05) when compared with the control. There were no statistically significant changes in MCV, MCH, MCHC, Monocytes, Eosinophils and Basophils in all treated groups compared to the control. Neutrophils was significantly decreased in group treated with 750mg/kg compared with control (P&gt; 0.05). The results of this study indicated that at lower doses, the aqueous leaf extract of <em>Jatropha tanjorensis</em> leaves may enhance haemopoiesis, but administration of higher dosage may cause haemolysis.</p><p><strong>Keywords:</strong> <em>Jatropha tanjorensis</em>, Haematological indices, WBC, RBC, Platelets, Haemolysis</p> 2020-01-30T00:00:00+00:00 Copyright (c) Preliminary investigation of the neuroprotective potentials of <i>Crossyne guttata</i> in MPP<sup>+</sup>-induced toxicity in SH-SY5Y 2020-01-30T15:02:45+00:00 S.I. Omoruyi A.B. Enogieru A.A. Hussein O.E. Ekpo <p>Parkinson's disease (PD) is a movement disorder caused by the gradual and sustained loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). There is presently no permanent treatment for PD, thus the need for more investigations into complementary and alternative medicine capable of inhibiting neuronal damage. This study investigates the potential neuroprotective activity of <em>Crossyne guttata</em>, a plant commonly found in the western and southern Cape of South Africa in 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>)-induced, <em>in vitro</em> model of PD, using the SH-SY5Y neuroblastoma cells.</p><p><strong>Methodology:</strong> The optimal concentration of <em>Crossyne guttata</em> aqueous extract (CGE) that showed no toxicity on cells and the concentration of MPP<sup>+</sup> that reduced cell viability to about 50% was determined using the 3-(4,5-dimethyithiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Following this SH-SY5Y cells were pretreated with 10 μg/ml of CGE for 2 hours before the addition of 2000 μM of MPP<sup>+</sup> and cell survival was determined. Furthermore, morphological changes associated with treatments were observed under the light microscope.</p><p><strong>Results:</strong> Results show that CGE did not reduce cell viability in the cells at all concentrations tested, while MPP<sup>+</sup> showed a dose-dependent reduction in cell viability. Also, pretreatment of cells with CGE extract improved cell survival as well as cell morphology by inhibiting toxicity induced by MPP<sup>+</sup>.</p><p><strong>Conclusion:</strong> Findings from this study suggest that CGE may be a potential neuroprotective agent in PD and thus make a case for further investigation into the mechanism(s) of action as well as bioactive components of the plant eliciting such effects.</p><p><strong>Keywords:</strong><em> Crossyne guttata</em>, Medicinal plants, 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>), Cell viability</p> 2020-01-30T00:00:00+00:00 Copyright (c)