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  <title>Digital Knowledge Community:</title>
  <link rel="alternate" href="http://hdl.handle.net/11189/490" />
  <subtitle />
  <id>http://hdl.handle.net/11189/490</id>
  <updated>2026-09-22T23:29:43Z</updated>
  <dc:date>2026-09-22T23:29:43Z</dc:date>
  <entry>
    <title>Investigation of haematological, inflammatory parameters and the incidence of alloimmunization in multi-transfused sickle cell diseased patients</title>
    <link rel="alternate" href="http://hdl.handle.net/11189/10856" />
    <author>
      <name>Aboderin, Florence</name>
    </author>
    <author>
      <name>Oduola, Taofeeq</name>
    </author>
    <author>
      <name>Davison, Glenda Mary</name>
    </author>
    <author>
      <name>Oguntibeju, Oluwafemi</name>
    </author>
    <id>http://hdl.handle.net/11189/10856</id>
    <updated>2026-09-22T20:45:27Z</updated>
    <published>2025-01-01T00:00:00Z</published>
    <summary type="text">Title: Investigation of haematological, inflammatory parameters and the incidence of alloimmunization in multi-transfused sickle cell diseased patients
Authors: Aboderin, Florence; Oduola, Taofeeq; Davison, Glenda Mary; Oguntibeju, Oluwafemi
Abstract: Introduction: Sickle cell disease is a haemoglobinopathy caused by an aberrant mutation of the beta chain with the amino acid valine replacing glutamic acid at the 6th position. Patients with sickle cell disease suffer from complications including chronic inflammation and the development of allogeneic antibodies due to multiple blood transfusions. This study investigated the association between haematological, inflammatory markers and alloimmunization in multi-transfused patients with sickle cell disease. Methods: This was a cross-sectional study, that enrolled 100 participants; 50 young adults (18−48 years) with homozygous sickle cell disease (Sickle cell Group) from the Obafemi University Health Centre in Nigeria, and 50 age and sex matched individuals who did not have the disease (Control group) but who had also received blood transfusions. Complete blood counts and differentials were processed on an auto-analyser (SFRI H18 Light, France). Red cell antigen identification used the saline and anti-human globin method while the abnormal haemoglobinopathy was evaluated using electrophoresis. ABO and Rhesus blood groups were analysed using a direct method ontile, andthedetermination ofinflammatory markers including C-reactive protein, tumour necrosis factor-alpha, interleukin-6, and interleukin-1b was by the enzyme-linked immunosorbent assay technique. The data were statistically analysed using SPSS version 24.0 and GraphPad Prism. Additionally, the student t-test and Chi-square test were employed as appropriate. Data were presented as mean§standarddeviation, with ap-value &lt;0.05 considered statistically significant. Result: As expected, the Sickle Cell group had an increased rate of alloimmunisation and significantly reduced haemoglobin and red cell parameters except for the mean cell volume. Although both groups had platelet counts within the reference range the Sickle Cell group had significantly higher counts than the Control group. The Sickle Cell group displayed evidence of inflammation with significantly increased levels (p-value = 0.001) of C-reactive protein and tumour necrosis factor-alpha. This was supported by higher white cell counts and neutrophilia. The majority of the antibodies detected in sickle cell disease were anti-Kell, Jka and Fya while the controls showed a higher prevalence of anti-M and Kell antibodies. Despite the elevated inflammatory markers, no significant correlation was observed between these and the rate of alloimmunization. Conclusion: In this study, the Sickle Cell group had an elevated rate of alloimmunization with higher levels of anti-kell, Jka and Fya as well as inflammatory markers. However, despite these findings, no significant correlation between inflammatory markers and alloimmunization could be detected. This suggests that elevated alloimmunization rates are multifactorial and involve other processes which require further investigation.</summary>
    <dc:date>2025-01-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Silymarin attenuates cobalt chloride-induced redox imbalance and cardio-renal dysfunctions in rats</title>
    <link rel="alternate" href="http://hdl.handle.net/11189/10855" />
    <author>
      <name>Ajibade, Temitayo Olabisi</name>
    </author>
    <author>
      <name>Ohore, Okezi Michael</name>
    </author>
    <author>
      <name>Esan, Oluwaseun Olarenwaju</name>
    </author>
    <author>
      <name>Adeoye, Bisi Olajumoke</name>
    </author>
    <author>
      <name>Ake, Ayodele Stephen</name>
    </author>
    <author>
      <name>Adetona, Moses Olusola</name>
    </author>
    <author>
      <name>Awoyomi, Omolola Victoria</name>
    </author>
    <author>
      <name>Igado, Olumayowa Olawumi</name>
    </author>
    <author>
      <name>Oyagbemi, Taiwo Olaide</name>
    </author>
    <author>
      <name>Adeogun, Adewunmi Victoria</name>
    </author>
    <author>
      <name>Oyagbemi, Ademola Adetokunbo</name>
    </author>
    <author>
      <name>Omobowale, Temidayo</name>
    </author>
    <author>
      <name>Oguntibeju, Oluwafemi Omoniyi</name>
    </author>
    <author>
      <name>Nwulia, Evaristus</name>
    </author>
    <author>
      <name>Audu Yakubu, Momoh</name>
    </author>
    <id>http://hdl.handle.net/11189/10855</id>
    <updated>2026-09-17T20:51:54Z</updated>
    <published>2025-01-01T00:00:00Z</published>
    <summary type="text">Title: Silymarin attenuates cobalt chloride-induced redox imbalance and cardio-renal dysfunctions in rats
Authors: Ajibade, Temitayo Olabisi; Ohore, Okezi Michael; Esan, Oluwaseun Olarenwaju; Adeoye, Bisi Olajumoke; Ake, Ayodele Stephen; Adetona, Moses Olusola; Awoyomi, Omolola Victoria; Igado, Olumayowa Olawumi; Oyagbemi, Taiwo Olaide; Adeogun, Adewunmi Victoria; Oyagbemi, Ademola Adetokunbo; Omobowale, Temidayo; Oguntibeju, Oluwafemi Omoniyi; Nwulia, Evaristus; Audu Yakubu, Momoh
Abstract: Silymarin is an extract of Silybum marianum that is used traditionally for the treatment of several diseases. This study sought to evaluate the protective effects of silymarin on cobalt chloride (CoCl2)-induced cardio-renal toxicities in rats. Forty rats were randomly divided into four groups of 10 rats each: control; 300 mg/kg CoCl2; CoCl2 + 100 mg/kg silymarin; and 100 mg/kg silymarin only. All administrations were done orally. At the end of the experimental period (seven days), blood pressure parameters, markers of oxidative stress, antioxidant defense status, renal function test, histopathology and immunohistochemical expressions were evaluated on the heart and kidney tissues. Silymarin significantly (p &lt; 0.05) altered CoCl2-induced alterations in blood pressure parameters, antioxidants and markers of oxidative stress, blood urea nitrogen and creatinine. Histopathological evaluation revealed area of infiltration of the myocardium by inflammatory cells and hemorrhages in the kidney of rats exposed to CoCl2 without silymarin treatment, but these lesions were absent in the control and silymarin groups. Increased immunohistochemical expression of cardiac troponin I and matrix metalloproteinase-2 (MMP-2) was observed in the cardiac tissues of rats exposed to CoCl2 without silymarin treatment. The immunohistochemical expression of cystatin C was heightened, while that of angiotensin-converting enzyme 2 (ACE2) was attenuated in the CoCl2 untreated group compared with the control and silymarin groups. In conclusion, silymarin effectively mitigated the toxic effects of CoCl2 on the heart and kidney tissues of rats due to its ability to positively modulate the activities of endogenous antioxidants and neutralize reactive oxygen species in cardiac and renal systems.</summary>
    <dc:date>2025-01-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Epigallocatechin -3- gallate mitigates diazinon neurotoxicity via suppression of pro-inflammatory genes and upregulation of antioxidant pathways</title>
    <link rel="alternate" href="http://hdl.handle.net/11189/10854" />
    <author>
      <name>Onukak, Charles Etang</name>
    </author>
    <author>
      <name>Femi-Akinlosotu, Omowumi Moromoke</name>
    </author>
    <author>
      <name>Obasa, Adedunsola Adewunmi</name>
    </author>
    <author>
      <name>Folarin, Oluwabusayo Racheal</name>
    </author>
    <author>
      <name>Ajibade, Temitayo Olabisi</name>
    </author>
    <author>
      <name>Igado, Olumayowa Olawumi</name>
    </author>
    <author>
      <name>Esan, Oluwaseun Olarenwaju</name>
    </author>
    <author>
      <name>Oyagbemi, Taiwo Olaide</name>
    </author>
    <author>
      <name>Adeogun, Adewumi Victoria</name>
    </author>
    <author>
      <name>Oyagbemi, Ademola Adetokunbo</name>
    </author>
    <author>
      <name>Ola-Davies, Olufunke Eunice</name>
    </author>
    <author>
      <name>Omobowale, Temidayo Olutayo</name>
    </author>
    <author>
      <name>Olopade, James Olukayode</name>
    </author>
    <author>
      <name>Oguntibeju, Oluwafemi</name>
    </author>
    <author>
      <name>Audu Yakubu, Momoh</name>
    </author>
    <id>http://hdl.handle.net/11189/10854</id>
    <updated>2026-09-17T20:45:29Z</updated>
    <published>2025-01-01T00:00:00Z</published>
    <summary type="text">Title: Epigallocatechin -3- gallate mitigates diazinon neurotoxicity via suppression of pro-inflammatory genes and upregulation of antioxidant pathways
Authors: Onukak, Charles Etang; Femi-Akinlosotu, Omowumi Moromoke; Obasa, Adedunsola Adewunmi; Folarin, Oluwabusayo Racheal; Ajibade, Temitayo Olabisi; Igado, Olumayowa Olawumi; Esan, Oluwaseun Olarenwaju; Oyagbemi, Taiwo Olaide; Adeogun, Adewumi Victoria; Oyagbemi, Ademola Adetokunbo; Ola-Davies, Olufunke Eunice; Omobowale, Temidayo Olutayo; Olopade, James Olukayode; Oguntibeju, Oluwafemi; Audu Yakubu, Momoh
Abstract: Diazinon is a commonly used organophosphate (OP) insecticide especially in developing countries for the control of insect pests, however, exposure to its toxic impact especially in humans and other non-target species remains an important public health concern. The study aimed to investigate the effect of epigallocatechin -3- gallate (EGCG), abundant in green tea plants on neurobehavioural, biochemical, and pathological changes in the brain of male Wistar rats following exposure to diazinon toxicity. Sixty adult male Wistar rats were acclimatized for seven days and subsequently randomly assigned into six treatment groups as follows: Group I: Control group (0.2 mL distilled water); Group II: Diazinon at 3 mg/kg (1% LD50); Group III: Diazinon (3 mg/kg) + EGCG (50 mg/kg, ~ 2% of LD50); Group IV: Diazinon (3 mg/kg) + EGCG (100 mg/kg, ~ 5% of LD50); Group V: EGCG (50 mg/kg) and Group VI: EGCG (100 mg/kg). All treatments were administered orally once daily for 14 days. Neurobehavioural studies, biomarkers of oxidative stress, histology, immunohistochemistry, and quantitative polymerase chain reaction (RT qPCR) were performed. Diazinon alone impaired recognition memory, increased oxidative stress markers and altered antioxidant defense in the brain. It upregulated TNF-α and IL-6 genes and repressed GPx 4 gene expressions. It was also associated with increased GFAP, Tau, and α-SN immunoreactivity. Microscopic examination revealed loss of Purkinje and hippocampal cells in brain. Co-treatment with EGCG however improved cognition, lowered oxidative stress markers, improved antioxidant status and suppressed TNF-α and IL-6. In conclusion, findings from this study demonstrated that EGCG offered protection against diazinon-induced neurotoxicity. Hence, natural sources of epigallocatechin -3- gallate such as fruits and vegetables could offer immense benefits by protecting against oxidative stress and inflammation in neurodegenerative disease conditions.</summary>
    <dc:date>2025-01-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Methanol leaf extract of Azadirachta indica mitigates isoproterenol-induced myocardial infarction through the modulation of oxidative stress, and PPARα and BCL2 signaling in rats</title>
    <link rel="alternate" href="http://hdl.handle.net/11189/10853" />
    <author>
      <name>Yusuf, Amirah</name>
    </author>
    <author>
      <name>Ajibade, Temitayo</name>
    </author>
    <author>
      <name>Esan, Oluwaseun</name>
    </author>
    <author>
      <name>Asenuga, Ebunoluwa Racheal</name>
    </author>
    <author>
      <name>Onoja, Moyinoluwa</name>
    </author>
    <author>
      <name>Akpan, Matthew</name>
    </author>
    <author>
      <name>Badejo, Joseph</name>
    </author>
    <author>
      <name>Omobowale, Temidayo</name>
    </author>
    <author>
      <name>Oyagbemi, Ademola Adetokunbo</name>
    </author>
    <author>
      <name>Adedapo, Adeolu</name>
    </author>
    <author>
      <name>Oguntibeju, Oluwafemi</name>
    </author>
    <author>
      <name>Audu Yakubu, Momoh</name>
    </author>
    <id>http://hdl.handle.net/11189/10853</id>
    <updated>2026-09-17T20:52:15Z</updated>
    <published>2025-01-01T00:00:00Z</published>
    <summary type="text">Title: Methanol leaf extract of Azadirachta indica mitigates isoproterenol-induced myocardial infarction through the modulation of oxidative stress, and PPARα and BCL2 signaling in rats
Authors: Yusuf, Amirah; Ajibade, Temitayo; Esan, Oluwaseun; Asenuga, Ebunoluwa Racheal; Onoja, Moyinoluwa; Akpan, Matthew; Badejo, Joseph; Omobowale, Temidayo; Oyagbemi, Ademola Adetokunbo; Adedapo, Adeolu; Oguntibeju, Oluwafemi; Audu Yakubu, Momoh
Abstract: Objective: Evaluation of Azadirachta indica’s potential on the modulation of blood pressure parameters, antioxidant defense status, as well as immunohistochemical expressions of Peroxisome proliferator-activated receptor α (PPARα) and Bcl-2 (B-cell lymphoma 2) in rats exposed to isoproterenol was the objective of this study.&#xD;
Materials and Methods: Fifty rats (Rattus norvegicus) of the Wistar strain were used, with myocardial infarction induced by intraperitoneal administration of isoproterenol (ISO) for two consecutive days. Cardiac and renal biomarkers of oxidative stress, blood pressure parameters, electrocardiography, and immunohistochemical staining of PPARα and BCL2 were performed.&#xD;
Results: ISO toxicity heightened blood pressure parameters, aggravated oxidative processes, declined antioxidant defense system, and decreased immunohistochemical expressions of PPARα and BCL2. Interestingly, A. indica improved antioxidant status, lowered free radical generation, mitigated serum myeloperoxidase and xanthine oxidase activities, respectively.&#xD;
Conclusion: Mitigation of oxidative mechanisms and antihypertensive effects of Azadirachta indica suggest a positive modulatory role for the medicinal plant in isoproterenol-induced myocardial infarction.</summary>
    <dc:date>2025-01-01T00:00:00Z</dc:date>
  </entry>
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