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1.
Eur Rev Med Pharmacol Sci ; 28(2): 805-813, 2024 Jan.
Article in English | MEDLINE | ID: mdl-38305623

ABSTRACT

OBJECTIVE: Doxorubicin (DXR) is commonly used as a drug for cancer treatment. However, there have been reports of neurotoxicity associated with chemotherapy. Galantamine (GLN) is a medication that inhibits cholinesterase activity, providing relief from the neurotoxic effects commonly seen in individuals with Alzheimer's disease. This study explored the potential ameliorative effect of GLN on brain neurotoxicity induced by DXR. MATERIALS AND METHODS: Forty rats were allocated into four separate groups for a study that lasted for a period of fourteen days. The control group was given normal saline, DXR group was given 5 mg/kg DXR every three days (cumulative dose of 20 mg/kg) through intraperitoneal injection. The GLN group was given 5 mg/kg GLN through oral gavage daily, while the DXR+GLN group was given DXR+GLN simultaneously. An analysis of brain proteins using ELISA to assess apoptosis through the concentration of inflammation and oxidative injury markers. RESULTS: The DXR treatment led to increased neuroinflammation by elevation of nuclear factor kappa B (NF-κB), and cyclooxygenase-2 (COX-2), oxidative stress by rise of malondialdehyde (MDA), and decline of superoxide dismutase (SOD), and no changes in catalase and glutathione (GSH), cell death by elevation of Bax and caspase-3 and reduced Bcl-2, and increase lipid peroxidation, impaired mitochondrial function. When GLN is administered alongside DXR, it has been observed to positively impact various biological markers, including COX-2, NF-κB, MDA, SOD, Bax, Bcl-2, and caspase-3 levels. Additionally, GLN improves lipid peroxidation and mitochondrial activity. CONCLUSIONS: DXR therapy in rats results in the development of neurotoxicity, and a combination of GLN can recover these toxicities, suggesting GLN promising evidence for mitigating the neurotoxic effects induced by DXR.


Subject(s)
Galantamine , NF-kappa B , Rats , Animals , Galantamine/pharmacology , Caspase 3/metabolism , bcl-2-Associated X Protein/metabolism , NF-kappa B/metabolism , Neuroinflammatory Diseases , Cyclooxygenase 2/metabolism , Oxidative Stress , Doxorubicin/toxicity , Glutathione/metabolism , Apoptosis , Proto-Oncogene Proteins c-bcl-2/metabolism , Superoxide Dismutase/metabolism
2.
Eur Rev Med Pharmacol Sci ; 27(14): 6480-6488, 2023 Jul.
Article in English | MEDLINE | ID: mdl-37522659

ABSTRACT

OBJECTIVE: The long-term consequences of congenital diaphragmatic hernia (CDH), which include altered lung functions and compromised cardiopulmonary capacity, impact functional performance and quality of life. This study investigates the effects of virtual reality-based exercise programs on pulmonary functions, cardiopulmonary capacity, functional performance, and quality of life in children with repaired CDH. PATIENTS AND METHODS: A randomized controlled clinical trial was performed. Fifty-two children with repaired CDH (aged 6-10 years) were enrolled and randomly allocated to virtual reality-based exercises plus traditional physical therapy (VR-EX group, n = 26) or traditional physical therapy alone (control group, n = 26). Interventions were conducted three times a week for 12 weeks. Pulmonary functions, cardiopulmonary capacity, functional performance, and quality of life were assessed before and after the intervention. RESULTS: The VR-EX group demonstrated significantly enhanced post-treatment pulmonary functions and cardiopulmonary capacity compared to the control group after accounting for the pre-treatment values (p < 0.05). In addition, the values in functional performance and quality of life measures showed significantly larger improvements in the VR-EX group (p < 0.05). CONCLUSIONS: Children with repaired CDH may benefit more from VR-based exercises when combined with traditional physical therapy than from traditional physical therapy alone regarding their pulmonary functions, cardiopulmonary capacity, functional performance, and quality of life.

3.
Eur Rev Med Pharmacol Sci ; 26(6): 2106-2116, 2022 03.
Article in English | MEDLINE | ID: mdl-35363360

ABSTRACT

OBJECTIVE: Aspirin resistance is described as the failure of aspirin to decrease the production of thromboxane A2 by platelets, which is the mechanism by which aspirin decreases platelet activation and aggregation. This study was performed to assess the prevalence of aspirin resistance among cardiovascular patients in al-Qassim, Saudi Arabia. PATIENTS AND METHODS: The study used a survey of patients with first and recurrent attacks of ischemic heart disease (IHD) and available data from blood samples processed using a VerifyNow® kit, which measures aspirin reaction units (ARUs). RESULTS: A total of 119 patients were included: 45 with their first IHD episodes and 74 with recurrent episodes. Of the surveyed patients, 40% with a first episode were younger than 50 years old, and 75.6% of them have been diagnosed with IHD during the previous 5 years. Of the patients with recurrent attacks, 45.9% were older than 60 years, and 54.1% of them have been diagnosed more than 5 years before. The group with first episodes of IHD had 133.2 ARUs, whereas the group with recurrent episodes had 168.5 ARUs (p=0.105). In the recurrent-episode group, 77% had diabetes; in the first-episode group, only 37.8% had diabetes (p≤0.001). Overall, 46.2% were overweight, 54.6% were nonsmokers, and 82.4% underwent percutaneous coronary intervention. CONCLUSIONS: The study participants in both the new and recurrent IHD groups showed no sign of aspirin resistance. The presence of cardiovascular risk factors increased the likelihood of episode recurrence.


Subject(s)
Myocardial Ischemia , Platelet Aggregation Inhibitors , Aspirin/pharmacology , Blood Platelets , Drug Resistance , Humans , Middle Aged , Myocardial Ischemia/drug therapy , Myocardial Ischemia/epidemiology , Platelet Aggregation , Platelet Aggregation Inhibitors/pharmacology , Saudi Arabia/epidemiology
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