<?xml version="1.0" encoding="UTF-8"?>
<rss xmlns:dc="http://purl.org/dc/elements/1.1/" version="2.0">
  <channel>
    <title>DSpace Community: Department of Physiology</title>
    <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/7</link>
    <description>Department of Physiology</description>
    <pubDate>Sat, 28 Feb 2026 23:19:11 GMT</pubDate>
    <dc:date>2026-02-28T23:19:11Z</dc:date>
    <item>
      <title>EFFECTS OF ACUTE CHRONIC ADMINISTRATION OF ETHANOL EXTRACT OF Cola nitida SCHOTT AND ENDLICHER (KOLANUT) AND CAFFEINE ON GLUCOSE METABOLISM IN RATS</title>
      <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/906</link>
      <description>Title: EFFECTS OF ACUTE CHRONIC ADMINISTRATION OF ETHANOL EXTRACT OF Cola nitida SCHOTT AND ENDLICHER (KOLANUT) AND CAFFEINE ON GLUCOSE METABOLISM IN RATS
Authors: AFOLABI, O.A.
Abstract: Cola nitida is known for its high caffeine content. Caffeine administration has been shown to cause glucose intolerance and insulin resistance. However, few studies on the effect of kolanut and decaffeinated kolanut on glucose metabolism. This study was designed to investigate the effect of acute and chronic administration of Ethanol Extract of Kolanut (EEK) and Decaffeinated Ethanol Extract of Kolanut (DEEK) on glucose metabolism in Wistar rats. Kolanut was obtained from Ilobu, Osun State and authenticated at Department of Applied Biology, LAUTECH, Ogbomoso with herbarium number LHO 442. The seeds (500 g) were air-dried, powdered and macerated in cold ethanol. Decaffeination was achieved by soaking equal amount of the seeds in distilled water and adding dichloromethane. Caffeine content of EEK and DEEK was analysed using Gas Chromatography-Mass Spectrometry (GC-MS). In acute studies, 24 Wistar rats (235-300 g) divided into 4 groups were orally administered single dose of caffeine (6 mg/Kg), EEK (6 mg/Kg), DEEK (6 mg/Kg), and 0.3 mL distilled water (control). Sample collection commenced 30 minutes after administration. In chronic studies, the same doses were orally administered daily for eight weeks to another set of 24 rats (240-310g). Samples were collected a day after the final dose was given. In both phases, oral glucose tolerance test was carried out using standard procedure and the Areas Under Curve (AUC) calculated. Blood samples (0.2 mL) and liver biopsies were taken from each animal to determine insulin levels. Liver Glycogen Synthase (LGS), and phosphorylase activities using ELISA. Plasma glucose was determined using glucose oxidase method. Glycogen level was determined spectophotometrically by anthrone method. Data were subjected to descriptive statistics and analysed using ANOVA and Student t-test at α0.05. The GC-MS revealed caffeine content of 17.5% and 3.3% in the EEK and DEEK respectively. In the acute study, AUCᵍˡᵘᶜᵒˢᵉ. AUCᶦⁿˢᵘˡᶦⁿ increased by 19.0% and 11.8% for caffeine and EEK, respectively while DEEK had no effect on AUCᵍˡᵘᶜᵒˢᵉ. The AUCᶦⁿˢᵘˡᶦⁿ increased by 66.6%, 21.5% and 10.6% for caffeine, EEK, and DEEK, respectively. The liver glycogen content significantly decreased from 2.4±0.1 (control) to 1.1±0.1 and 1.3±0.2g/100g for caffeine and EEK, respectively while DEEK showed no effect. Acute administration of caffeine and EEK significantly decreased the activities of LGS and phosphorylase while DEEK had no effect. Chronic caffeine treatment increased AUCᵍˡᵘᶜᵒˢᵉ&#xD;
by 9.2% while EEK reduced AUCᵍˡᵘᶜᵒˢᵉ by 3.2% and DEEK had no effect. Caffeine increased AUCᶦⁿˢᵘˡᶦⁿ from 131.4±5.2 to 157.1±6.9 ng.min/mL, while EEK reduced AUCᶦⁿˢᵘˡᶦⁿ to 114.5±5.6 ng.min/mL, DEEK had no effect on AUCᶦⁿˢᵘˡᶦⁿ. Caffeine and DEEK had no significant effects on LGS and phosphorylase activities. On the contrary, EEK increased liver glycogen content from 1352.0±253.1 to 1987.8±304.9 mg/100g, and LGS activities from 1270.0±154.4 to 2470.0±229.9 ng/mg protein while the phosphorylase activities reduced from 21.3±1.1 to 17.6±0.9 ng/mg protein. Chronic administration of ethanol extract of kolanut enhanced glucose tolerance and insulin sensitivity while its acute administration resulted in glucose intolerance and insulin resistance. Decaffeination had no effect on insulin sensitivity and glucose tolerance.
Description: A Thesis in the Department of Physiology submitted to the Faculty of Basic Medical Sciences, College of Medicine in partial fulfillment of the requirements for the award of degree of Doctor of Philosophy of the University of Ibadan, Nigeria.</description>
      <pubDate>Tue, 01 Dec 2015 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://adhlui.com.ui.edu.ng/jspui/handle/123456789/906</guid>
      <dc:date>2015-12-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>REVERSAL OF SODIUM ARSENITE-INDUCED DELAY IN GASTRIC ULCER HEALING IN RATS BY KOLAVIRON, VITAMIN E AND ZINC</title>
      <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/903</link>
      <description>Title: REVERSAL OF SODIUM ARSENITE-INDUCED DELAY IN GASTRIC ULCER HEALING IN RATS BY KOLAVIRON, VITAMIN E AND ZINC
Authors: ADEBAYO, G. I.
Abstract: Arsenic acid is a major contaminant of various water sources used for human consumption and industrial activities in most developing countries. It has been reported to cause degenerative inflammation and oxidative damage in many tissues. However, there is a paucity of information on its effect on various gastrointestinal tract conditions of exposed individuals. A mechanistic study in rats on the ameliorative activities of antioxidants (kolaviron, zinc, and vitamin E) on the effects of Sodium Arsenite (SA) exposure during acetic acid - induced gastric ulcer healing was undertaken. &#xD;
Wistar rats (n= 125,150-200g), randomly divided into five groups were treated for two weeks as follows: control (distilled water), SA (5 mg/kg, p.o), SA+ kolaviron (100 mg/kg, p.o), SA+ vitamin E (100mg/kg, p.o), SA + zinc sulphate (20mg/kg p.o). Kolaviron was obtained from Garcinia Kola using soxhlet extraction process. Gastric ulceration was induced by administration of acetic acid (0.06 ml, 40 % v/v). Indices of ulcer healing determined on days 3, 7,14 and 21 post induction were ulcer score and area using planimetry, total gastric acidity by titration, and neutrophil/inflammatory cell infiltration using histomorphometry. Blood cells were quantified using haemoeytometry and activities of Superoxide Dismutase (SOD), Catalase, protein level, Malondialdehyde and Nitric oxide (NO) concentration were determined by spectrophotometry. Stomach sections were immunostained for CD 31 and Factor VIII (angiogenesis), p53 (apoptosis), Epidermal Growth Factor Receptor (EGFR) and Ki-67 (cell proliferation). Stomach tissue was also stained with H&amp;E, and viewed under light microscope. All these variables were evaluated by days 3,7,14 and 21 post-induction. Data were analysed using ANOVA at alpha 0.05. In the ulcerated control animals, the ulcer areas were 0.74 ± 0.01cm², 0.57 ± 0.08cm², 033 p  ± 0.12cm² and 0.24 ± 0.04 cm² while SA exposure significantly increased ulcer areas for 81.0%, 100.0%, 65.0%, 33.0% by days 3, 7, 14 and 21, respectively. By day 21 post-ulcer induction, zinc, Kolaviron and vitamin E had reduced ulcer areas relative to SA-treated group by 21.0%, 0.5% and 2.0%, respectively. Sodium arsenite decreased gastric mucosal thickness and parietal cell mass but increased lipid peroxidation, malondialdehyde levels and Neutrophil-Lymphocyte ratio. These affects were reversed by vitamin E and kolaviron. Total gastric acidity reduced while the levels of SOD, catalase, total protein and NO increased as healing progressed in all groups, but at a higher rate in the SA exposed group. The expression of CD31, factor VIII, Ki67 and EGFR proteins were significantly reduced by sodium arsenite, co-treatment with the antioxidants increased the labelling indices towards control values in the order zinc&gt;kolaviron&gt;vitamn E. The p53 expression was increased in SA treated animals but was reduced by the antioxidants in the same order. Gastric tissue necrosis, hyperplasia and haemorrhage observed in the SA-treated animals were reduced by the antioxidants. Sodium arsenite delayed gastric ulcer healing in rats via oxidative stress, inflammation, alteration in proliferative and apoptotic activities and impaired angiogenesis in the stomach.
Description: A Thesis in the Department of Physiology submitted to the Faculty of Basic Medical Sciences in partial fulfillment of the requirements for the Degree of Doctor of Philosophy of the University of Ibadan, Nigeria.</description>
      <pubDate>Thu, 01 Jun 2017 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://adhlui.com.ui.edu.ng/jspui/handle/123456789/903</guid>
      <dc:date>2017-06-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>EFFECTS OF KOLAVIRON AND THE BIFLAVANONES OF (garcinikola on acetic acid-incuced coltis in wistar rats)</title>
      <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/899</link>
      <description>Title: EFFECTS OF KOLAVIRON AND THE BIFLAVANONES OF (garcinikola on acetic acid-incuced coltis in wistar rats)
Authors: IGE, S.F
Abstract: Ulcerative colitis, a chronic inflammatory bowel disease, is characterized by inflammation, ulceration and increased colonic production of reactive oxygen species. Agents with anti-inflammatory property may be administered to ameliorate the symptoms. Kolaviron, a complex biflavonoid from Garcinia kola seeds, is known to possesses anti inflammatory and free radical scavenging properties. Previous reports have shown that kolaviron possess anti-colitis effects, with little information on its mechanism of action. The study was designed to investigate the possible mechanisms of action of kolaviron and its constituents- Garcinia biflavonone-1 (GB1), Garcinia biflavonone-2 (GB2) and kolaflavanone, on acetic acid-induced colitis in wistar rats. &#xD;
Thirty male Wistar rats (160 -200g) were assigned to six groups of five rats each and treated as follows: Distilled Warier (DW) (0.5 mL100g). Kolaviron (100 mg/kg), GBI (100 mg/kg),GB2 (100 mg/kg) and Kolaflavanone (100 mg/kg). The sixth group served as normal control. After seven days of treatment, colitis was induced by intra-rectal administration of 7% acetic acid (1mL/200g) in it the rats except normal control and assessed 48-hours thereafter, based on symptoms of colitis such as weight loss and stool consistency using a diarrhoea store scale. Colonic lipid peroxidation, mycloperoxidase (MPO), Tumor Necrosis Factor-alpha (TNF-a). Leukotriene B (LTB4), Prostaglandin E₂ (PGE₂) and Nitric Oxide (NO) were measured spectrophotometricarlly. Colonic total Protein (TP), Catalase (CAT), reduced glutathione (GSH) and Paraoxonase (PON) were measured using pathologically and scored microscopically. Data were analysed using descriptive statistics, ANOVA and Student t test at p⁼0.05. &#xD;
The diarrhoea scores in DW group (2.7±0.2) was significantly higher than the kolaviron (0.3±0.2) GBI (1.0±0.4) and GB2 (1.2±0.4) treated group. Kolaviron, GB1 and GB2 significantly reduced the weight loss. The gross (84.±4.2%) and microscopic  (3.6±0.2) colonic damages assessed in Dwgroup were significaantly reduced by kolaviron (29.6±9.6%, 2.0±0.5), GB1 (16.8±11%, 1.5±0.5) and GB2 (16.4±3.5%, 1.3±0.6). &#xD;
Kolaflavanone showed no significant effect on diarrhoea, weight loss and tissue damage. Lipid peroxidaiion level in the kolaviron (40.1±11.6 nmol/mg), GB1 (20.8±2.4 nmol/mg), GB2 (24.4±1.1 nmol/mg) were significantly lower than the DW group (94.9±6..9 nmol/mg). When compared to DW group, levels of MPO, TNF-a and NO were reduced in the order GB2 &gt; kolaviron &gt;GB1 . The TP was significantly increased by GB I and GB2 while kolaflavanone showed insignificant effect on lipid peroxidation, TP, MPO and TNF-a. The LTB₄ and PGE₂ levels in DW group (154.5±17.4 and 630±27.7 pg/mL)were significantly higher than in kolaviron (85.3±15.9, 212.2±41.5 pg/ml). GB I (8.8±18.5), 274.3±77.7 pg/ml), GB2 (12.3±2.4, 49.8± 11.4 pg/mL) and kolaflavanone (25.9±I2.9, 62.9±20.5 pg/ml) groups. Histology showed that severe epithelial damage evidenced by destruction of crypt architecture and loss of goblet cells in DW group were completely absent in GB2 and minimal in kolaviron and GB1 groups. &#xD;
Kolavirori and its constituents inhibited the acetic acid-induced inflammatory responses in colitis via oxidative stress-dependent mechanism by suppression of mycloperoxidase, tumor necrosis factor-alpha, leukotriene B, prostaglandin E₂ and nitric Oxide. Garcinia biflavanones-1 and -2 appear to be active constituents of Garcinia kola responsible for its anti-colitis efrfects. &#xD;
Keywords: Acetic acid-induced colitis, Garcinia kola, Pro-inflammaiory mediators. Garciniaflavanones &#xD;
word count: 499
Description: A thesis in the Department of Physiology submitted to the Faculty of Basic Medical Sciences, College of Medicine, in partial fulfillment of the requirements for the award of the degree of Doctor of Philosophy of the University of Ibadan, Nigeria.</description>
      <pubDate>Sat, 01 Aug 2015 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://adhlui.com.ui.edu.ng/jspui/handle/123456789/899</guid>
      <dc:date>2015-08-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>EFFECTS OF CHLOROFORM OF EXTRACT OF CARICA PAPAYA SEED ON PREGNANCY OUTCOME AND POSTNATAL DEVELOPMENT</title>
      <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/898</link>
      <description>Title: EFFECTS OF CHLOROFORM OF EXTRACT OF CARICA PAPAYA SEED ON PREGNANCY OUTCOME AND POSTNATAL DEVELOPMENT
Authors: Oyelowo, O.T
Abstract: Increasing frequency of reproductive disorders has been attributed to exposure to harmful exogenous substances during pregnancy. Studies have shown that Carica papaya seed inhibits fertility in Male and oestrous cycle of female rat. There is paucity of information on reproductive effects of C. papaya seed exposure during pregnancy and offspring development. The effect of Chloroform Extract of C papaya Seeds (CECS) and its purified compounds on pregnancy and offspring development were evaluated. Phytochemical analysis, acute toxicity and Gas Chromatography-Mass Spectroscopy (GCMS) of CECS were carried out using standard methods. Pregnant wistar rats (190-220g, n=110) were administered 50mg/kg CECS during the first (D7), second (D14) and third (D21) trimesters of pregnancy, Pre-coital group served as control and received 1Ml/kg olive oil. In another experiment (190-220g, n=25), pregnant rats were divided into three (first, second and third) trimesters and were continuously treated with 1000mg/kg of one of the purified compounds of CECS. Rats delivered naturally and pups were studied for post-natal variables from birth to puberty, Body weights, Anogenital Index (AGI), somatic and pubertal landmarks were measured using vernier calliper. Sperm motility, count and viability were assessed microscopically. Hormones (Testosterone, Luteinizing Hormone,. Follicle-Stimulating Hormone. Prolactin, Corticosterone) and antioxidants markers (Superoxide Dismutase and Glutathione Peroxidase) were measured by Enzyme lmmuno-sorbent assay and spectrophotometer respectively. Testicular histology was done using haematoxylin and eosin stains. Data were analysed using descriptive statistics, ANOVA and Student's t-test at p=0.05. &#xD;
1 Alkaloids, polyphenols, saponins. flavonoids were identified, while the GCMS analysis yielded oleic acid (40.7%). cis-13-octaderenoic acid (27.9%), cis-vaccenic acid (20.7%), trans-13-octadecenoic acid (6.0%), n-hexadecanoic acid (2.4%) and tetradecanoic acid (1.8%). There was no mortality with CECS treatment up to 3000mg/kg and OA treatment up to 2000mg/kg. Pregnancy outcome showed significant increase in gestation. length of OA treated dams. Litter sizes in CECS (7.5±0.1. 7.5±0.8, 5.5±0.9) and OA (5.5±0.9, 7.5±0.8, 5.50.9, 3.5±0.1) groups were significantly reduced when compared with the control (10.7±0.6). Body weight of CECS offspring significantly increased while OA offspring had alterations from birth to puberty. The AGI on post-natal D4 significantly reduced in OA (1.9±0.0) and CECS D14 (1.8±0.0) offspring when compared with the control (2.3±0.1). Significant delay occurred in day of eye opening and fur appearance in CECS and OA offspring. Puberty onset was significantly delayed in OA and CECS D14 offspring while CECS pretreated offspring had an earlier onset. Corticosterone level in OA, CECS pretreated offspring increased. Follicle-stimulating hormone significantly decreased in OA offspring and in CECS pretreatment and D14 offspring of treated dams. Luteinizing hormone was decreased in OA and increased in CECS offspring. Testosterone level, sperm motility, count and viability were significantly decreased in all offspring. Offspring treated with OA had reduced testicular prolactin level. The superoxide dismutase (3.9±0.1 and 2.8±0.0) and glutathione peroxidase (8.8±0.8 and 0. 6±0.0) were significantly reduced in CECS and OA offspring compared withcontrol (8.2±0.6 and 19.2±1.5) respectively. Continuous exposure of rat to chloroform extract of carica papaya seed and oleic acid for two trimesters showed foetotoxic effect.
Description: A thesis in the department of physiology submitted to the Faculty of Basic Medical Sciences, College of Medicine in partial fulfilment of the requirements for the degree of Doctor of Philosophy of the University of Ibadan, Nigeria.</description>
      <pubDate>Wed, 01 Jan 2014 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://adhlui.com.ui.edu.ng/jspui/handle/123456789/898</guid>
      <dc:date>2014-01-01T00:00:00Z</dc:date>
    </item>
  </channel>
</rss>

