We investigated the effects of β-glucan (βg) on kidney and liver damage caused by cisplatin (CP), an antineoplastic agent widely used to treat many types of cancer, in a rat model. The side effects of CP in many tissues and organs limit its usage. βg is a natural polysaccharide that is an effective free radical scavenger. A total of 28 rats were randomly divided into four groups. Group 1 was a non-intervention control, only feed and water were given. Group 2 was administered 7 mg/kg CP in a single dose. Group 3 was administered 50 mg/kg βg orally for 14 days. Group 4 was administered βg for 14 days, following a single dose of CP. At the end of the experiment, kidney and liver tissues were evaluated biochemically and histopathologically. Increased thiobarbituric acid-reactive substances (TBARS) levels, as well as decreased catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) levels, as well as histological damage, were noted in both the kidney and liver tissues of the CP group. However, βg treatment prevented the oxidative and histopathological effects of CP. The study demonstrates the protective efficacy of βg against CP-induced kidney and liver damage through the effect of its antioxidant properties.
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http://dx.doi.org/10.1080/10520295.2024.2320626 | DOI Listing |
Fluids Barriers CNS
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Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital of Southern Medical University, Guangzhou, 510515, China.
Oxidative stress and neuronal apoptosis could be an important factor leading to post-hemorrhagic consequences after germinal matrix hemorrhage (GMH). Previously study have indicated that relaxin 2 receptor activation initiates anti-oxidative stress and anti-apoptosis in ischemia-reperfusion injury. However, whether relaxin 2 activation can attenuate oxidative stress and neuronal apoptosis after GMH remains unknown.
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Department of Laboratory Animal Medicine, College of Veterinary Medicine, Jeonbuk National University, The 1st Veterinary R&D Building Rm 301, 79 Gobong-ro, Iksan-si, Jeollabuk-do, 54596, Republic of Korea.
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Graduate School of Biotechnology, and College of Life Science, Kyung Hee University, Yongin-Si, 17104, Gyeonggi-Do, Republic of Korea.
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Department of Pharmacotherapy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Introduction: Organ transplant recipients face a substantial risk of developing posttransplant lymphoproliferative disorders (PTLD). In over 90% of cases with B-cell PTLD following solid organ transplantation, the Epstein-Barr virus (EBV) genome is promptly identified, usually within the initial year. A continuing discussion revolves around the efficacy of antiviral prophylaxis in mitigating the incidence of PTLD in solid organ transplant (SOT) patients.
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APHP, Reference Center for Rare Diseases of Calcium and Phosphate Metabolism, and Filière OSCAR, endo ERN and ERN BOND, Paris, France.
X-linked hypophosphataemia (XLH) is a rare metabolic bone disorder caused by pathogenic variants in the PHEX gene, which is predominantly expressed in osteoblasts, osteocytes and odontoblasts. XLH is characterized by increased synthesis of the bone-derived phosphaturic hormone fibroblast growth factor 23 (FGF23), which results in renal phosphate wasting with consecutive hypophosphataemia, rickets, osteomalacia, disproportionate short stature, oral manifestations, pseudofractures, craniosynostosis, enthesopathies and osteoarthritis. Patients with XLH should be provided with multidisciplinary care organized by a metabolic bone expert.
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