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    <title>DSpace Collection: Dissertations in Pharmacology and Therapeutics</title>
    <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/698</link>
    <description>Dissertations in Pharmacology and Therapeutics</description>
    <pubDate>Sun, 05 Apr 2026 20:09:35 GMT</pubDate>
    <dc:date>2026-04-05T20:09:35Z</dc:date>
    <item>
      <title>EVALUATION OF ANTPSYCHOTIC EFFECTS OF METHYL JASMONATE IN MICE</title>
      <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/875</link>
      <description>Title: EVALUATION OF ANTPSYCHOTIC EFFECTS OF METHYL JASMONATE IN MICE
Authors: ANNAFI, O.S
Abstract: Psychosis is a chronic neurological disorder that impairs the quality of life of the patients and remains a major health challenge worldwide. Current drugs used to manage psychosis are expensive and only provide symptomatic relief without altering the underlying pathological derangement. Methyl jasmonate (MJ) is a bioactive compound known to have beneficial effects against a wide range of neurological disorders. However, its usefulness in treatment of psychosis has not been scientifically proven. Thus, this study was undertaken to investigate the effects of MJ on psychosis in animal models.&#xD;
Fifty male Swiss mice (23.5±1.5 g) were assigned to 10 groups to evaluate acute antipsychotic-like effect of MJ on bromocriptine or ketamine-induced stereotypy. Groups 1-5 received 1% ethanol (vehicle, 10 mL/kg, i.p.), MJ (25,  50,  100 mg/kg, i.p.) and haloperidol (1 mg/kg, p.o.) 60 minutes prior to bromocriptine (5 mg/kg, p.o.) treatment, while groups 6-10 received vehicle (10 mL/kg, i.p.), MJ (25,50,100 mg/kg, i.p.) and risperidone (0.5 mg/kg, p.o.) 60 minutes prior to ketamine injection. Thereafter, each mouse was placed independently in an observation chamber (20 cm × 20 cm × 23 cm) and stereotyped behaviours were observed for 2 min at 10, 15, 30, 45 and 60 min after bromocriptine or ketamine injection. Another 36 mice (n = 6) were also allotted into treatment groups. Group 1 received vehicle (10 mL/kg, i.p.) while groups 2-6 were treated with ketamine (20 mg/kg, i.p.) once daily, for 14 days. Then, from 8th to 14th day, group 2 was treated with vehicle (10 mL/kg, i.p.) while Group 3-6 received MJ (25,50.100 mg/kg, i.p.) and risperidone (0.5 mg/kg) 60 minutes after ketamine injection. Hyper-locomotion was then measured as an index of psychotic-like behaviour using the open field chamber while memory was assessed using the Y-maze. Thereafter, whole brain samples were used to assay for malondialdehyde, reduced glutathione (GSH), catalase and Superoxide Dismutase (SOD) using spectrophotometric techniques. Histology of prefrontal cortex, hippocampus and substantial nigra were viewed in ketamine-treated mice and neuronal density was determined. Data were analysed using descriptive statistics and ANOVA at α0.05.&#xD;
Methyl jasmonate (25, 50 and 100 mg/kg) significantly reduced stereotypy score (0.62±0.21, 0.24±0.10 and 0.06±0.04) relative to vehicle (1.84±0.15) and (0.50±0.08, 0.36±0.06, 0.26±0.07) relative to vehicle (1.52±0.10) induced by bromocriptine and ketamine, respectively. Methyl jasmonate significantly ameliorated ketamine-induced hyper-locomotion (74.67±4.70, 75.67±2.88, 78.00±4.16 s) compared to vehicle (185.0±3.63) and memory deficit (80.1±2.8, 71.2±2.9, 57.0±3.4 %) relative to vehicle (53.7±2.0%). Methyl jasmonate reduced malondialdehyde concentration (19.96±1.64, 22.84±1.16, 24.65±1.70 μmol/g tissue) relative to vehicle (33.72±2.28 μmol/g tissue) but increased GSH levels (47.43±2.22, 42.23±2.83, 37.26±1.84 μmol/g tissue) compared to vehicle (21.95± 2.69 μmol/g tissue).  Methyl jasmonate also increased catalase level in the brain homogenate  (86.63±4.65, 83.36±4.24, 76.06±3.22 units/mg protein) relative to vehicle (59.91±3.94 units/mg) and SOD (27.52±1.63, 24.41±1.49, 19.71±1.59 units/mg protein) compared with vehicle  (13.08±1.33 units/mg protein), respectively. Brain histology revealed that MJ has protective property on neuronal cells compared to ketamine-treated mice.&#xD;
Methyl jasmonate demonstrated antipsychotic property via activation of antioxidation pathway in Swiss mice.
Description: A dissertation submitted to the department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, University of Ibadan in partial fulfillment of the requirements for the award of the degree of Master of Philosophy (Pharmacology) of the University of Ibadan, Nigeria.</description>
      <pubDate>Sun, 01 Jan 2017 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://adhlui.com.ui.edu.ng/jspui/handle/123456789/875</guid>
      <dc:date>2017-01-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>EVALUATION OF ANTIPSYCHOTIC EFFECTS OF METHYL JASMONATE IN MICE</title>
      <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/844</link>
      <description>Title: EVALUATION OF ANTIPSYCHOTIC EFFECTS OF METHYL JASMONATE IN MICE
Authors: ANNAFI, O.S.
Abstract: Psychosis is a chronic neurological disorder that impairs the quality of life of the patients and remains a major health challenge worldwide. Current drugs used to manage psychosis are expensive and only provide symptomatic relief without altering the underlying pathological derangement. Methyl jasmonate (MJ) is a bioactive compound known to have beneficial effects against a wide range of neurological disorders. However, its use in treatment of psychosis has not been scientifically proven. Thus, this study was undertaken to investigate the effects of MJ on psychosis in animal models. &#xD;
Fifty male Swiss mice (23.5±1.5 g) were assigned to 10 groups to evaluate acute antipsychotic- Iike effect of MJ on bromocriptine or ketamine-induced stereotype. Groups 1-5 received 1% ethanol (vehicle, 10 mL/kg, i.p.) MJ (25, 50, 100 mg/kg, i.p.) and haloperidol (1 mg/kg, p.o.) 60 minutes prior to bromocriptine (5 mg/kg, p.o.) treatment, while groups 6-10 received vehicle (10 mL/kg, i.p.),MJ (25, 50,100 mg/kg, i.p,) and risperidone (0.5 mg/kg, p.o) 60 minutes prior to ketamine injection. Thereafter, each mouse was pIaced independently in an observation chamber (20 cm 20 cm x 23 cm) and stereotyped behaviours were observed for 2 min at 10, 15, 30, 45 and 60 min after bromocriptine or ketamine injection. Another 36 mice (n = 6) were also allotted into treatment groups. Group 1 received vehicle (10 mL/kg, i.p.) while groups 2-6 were treated with ketamine (20 mg/kg. i.p.) once daily for 14 days. Then, from 8th to 14th day, group 2 was treated with vehicle (10 mL/kg, i.p.) while Group 3-6 received MJ (25,50,100 mg/kg, i.p.) and risperidone (0.5 mg/kg) 60 minutes after ketamine injection. Hyper-locomotion was then measured as an index of psychotic-like behaviour using the open field chamber while memory was assessed using the Y-maze. Thereafter, whole brain samples were used to assay for malondialdehyde, reduced glutathione (GSH), catalase and Superoxide Dismutase (SOD) using spectrophotometric techniques. Histology of prefrontal cortex, hippocampus and substantial nigra were viewed in ketamine-treated mice and neuronal density was determined. Data were analysed using descriptive statistics and ANOVA at α0.05. Methyl jasmonate (25, 50 and 100 mg/kg) significantly reduced stereotype score (0.62±0.21, 0.24±0.10 and 0.06±0.04) relative to vehicle (1.84±0.15) and (0.50±0.08, 0.26±0.07) relative to vehicle (1.52±0.10) induced by bromocriptine and ketamine, respectively. Methyl jasmonate significantly ameliorated ketamine-induced hyper-locomotion (74.61±4.70, 75.67±2.88, 78.00±4.16 s) compared to vehicle (185.0±3.63) and memory deficit (80.1±2.8, 71.1±2.9, 57.0±3.4 %) relative to vehicle (53.7±2.0%). Methyl jasmonate reduced malondialdehyde concentration (19.96±1.64, 22.84±1.16, 24.65±1.70 umol/g tissue) relative to vehicle (33.71±2.28 umol/g tissue) but increased GSH levels (47.43±2.22, 42.23±2.83, 37.26±1.84 umol/g tissue) compared to vehicle (21.95± 2.69 umol/g tissue). Methyl jasmonate also increased catalase level in the brain homogenate (86.63±4.65, 83.36±4.24, 76.06±3.22 units/mg protein) relative to vehicle (59.91±3.94 units/mg) and SOD (27.52± 1.63, 24.41±1.49, 19.71±1.59 units/mg protein) compared with vehicle (13.08±1.33 units/mg protein) respectively. Brain histology revealed that MJ has protective property on neuronal cells compared to ketamine-treated mice. Methyl jasmonate demonstrated antipsychotic property via activation of antioxidation pathway in Swiss mice.
Description: A Dissertation submitted to the Department of Pharmacology and Therapeutics, Faculty of Basic and Medical Sciences in partial fulfillment of the requirements for the Degree of Master of Philosophy of the University of Ibadan, Nigeria.</description>
      <pubDate>Sun, 01 Jan 2017 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://adhlui.com.ui.edu.ng/jspui/handle/123456789/844</guid>
      <dc:date>2017-01-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>NEUROPHARMACOLOGICAL PROPERTIES OF ETHANOL EXTRACT OF THE LEAVES OF Olax subscorpioidea OLIV. (OLACACEAE) IN MICE</title>
      <link>http://adhlui.com.ui.edu.ng/jspui/handle/123456789/712</link>
      <description>Title: NEUROPHARMACOLOGICAL PROPERTIES OF ETHANOL EXTRACT OF THE LEAVES OF Olax subscorpioidea OLIV. (OLACACEAE) IN MICE
Authors: ADEOLUWA, O. A.
Abstract: Olax subscorpioidea is used in the management of mental illness, fever and pain in ethnomedicine. However, there is scanty information on the neuropharmacological activities that supports its use. The study was designed to investigate the neuropharmacological properties of Ethanol Extract of Olax subscorpioidea Leaves (EEOSL) in male mice. &#xD;
Air-dried leaves (150 g) were pulverized and soaked in 50% ethanol (1.5 L) for 48 hours. The filtrate was concentrated and evaporated to dryness (8.7 g). Twenty-five Swiss male albino mice (20-22 g) were allotted into five treatment groups viz: control (distilled water), and EEOSL (3.1, 6.3, 12.5, 25 mg/kg) with five animals in each group. They were pretreated thirty minutes intraperitioneally (i.p.). before neurobehavioural effects of EEOSL on novetty-induced behaviours (rearing and grooming) and frequency of head dips were investigated using open-field and hole-board tests respectively. Another twenty male mice (22-25 g) divided into four treatment groups: control (distilled water) and EEOSL (12.3, 25. 50 mg). Thirty minutes after i.p. treatment, pentobarbitone-induced sleeping t ime was investigated. For analgesic study, eighty male mice (22-25 g) were allocated into four treatment groups: control (distilled water), and EEOSL (12.5. 25, 50 mg/kg) with five animals in each group. Thirty minutes after i.p. treatment they were subjected to acetic-acid induced writhing, formalin, tail immersion and hot plate tests. Similarly, for antidepressant study, another set of eighty mate mice (22-25 g) were randomly allotted into four treatment groups; control (distilled water), and EEOSL (6.3, 12.5, 25 mg/kg) with five animals in each group. Thirty minutes after i.p. treatment, animals were subjected to despair, tail suspension, reserpine-induced depression, and yohimbine lethality tests. Data were analysed using descriptive statistics and ANOVA at p=0.05. &#xD;
The EEOSL (3.1, 6.3,12.5. 25 mg/kg) significantly inhibited rearing (99.8±2.8, 76.2±2.9, 37.4±1.2, 5.8±0.8) and grooming (48.0±3.6, 33.8±2.9, 25.4±1.6, 7.6:±0.8) compared with controls (185.8±5.1; 63.8±4.3) respectively. Treatment with EEOSL (3.125, 6.25, 12.5, 25 mg/kg significantly decreased the frequency of head dips on hole-board (10.6±1.9, 8.8±1.2, 7.2±0.9, 6.0±1.1) compared with control (27.8±1.5). The EEOSL (12.5, 25. 50 mg/kg) significantly prolonged pentobarbitone-induced sleeping time (43.0±1.4, 51.0±1.2, 61.0±1.8) compared with control (31.0±0.7). The EEOSL (12.5, 25, 50 mg/kg) significantly inhibited acetic acid-induced pain by 66.9%, 72.7% and 81.5% respectively. In formalin test, EESOL (12.5, 25, 50 mg/kg) inhibited neurogenic (41.1%, 63.1%. 66.0%) and inflammatory (57.1%, 75.3%, 79.4%) pains. Reaction times were prolonged only by EEOSL (50 mg/kg) in hot plate (0.9±0.1) and tail immersion (2.1±0.2) compared with controls (0.6±0.1; 0.5±0.0) respectively. The EEOL, (6.3, 12.5 mg/kg) significantly reduced immobility periods in despair (124.2±4.5, 85.2±6.0) and tail suspension tests (110.4±6.8, 68.0±15.9) compared with controls (190.2±15.3; 155.6±8.9) respectively. In reserpine-induced depression, EEOSL (6.3, 12.5, 25 mg/kg) reduced significantly the feacal matter (2.4±0.9, 1.2±0.6, 1.2±0.4) compared with control (8.2±0.9). However, EEOSL did not potentiate yohimbine-induced lethality. &#xD;
Olax subscorpioidea possessed sedative, antidepressant and analgesic properties. These therefore support its traditional claim in the management of mental illness and pain.
Description: A Dissertation submitted for the award of the degree of M.Phil in the Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences College of Medicine, University of Ibadan, Ibadan, Nigeria.</description>
      <pubDate>Tue, 01 Jul 2014 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://adhlui.com.ui.edu.ng/jspui/handle/123456789/712</guid>
      <dc:date>2014-07-01T00:00:00Z</dc:date>
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