Bioorganic & Medicinal Chemistry, Год журнала: 2024, Номер unknown, С. 118045 - 118045
Опубликована: Дек. 1, 2024
Язык: Английский
Bioorganic & Medicinal Chemistry, Год журнала: 2024, Номер unknown, С. 118045 - 118045
Опубликована: Дек. 1, 2024
Язык: Английский
Toxicology and Applied Pharmacology, Год журнала: 2025, Номер unknown, С. 117306 - 117306
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0Frontiers in Pharmacology, Год журнала: 2025, Номер 16
Опубликована: Апрель 1, 2025
Cerebral ischemia-reperfusion (CIR) injury critically impacts stroke prognosis, yet effective therapeutic strategies remain limited. Irisin, an exercise-induced myokine, exhibits neuroprotective effects against cerebral ischemia. SIRT3, a mitochondrial deacetylase, is similarly implicated in mitigating injury. Given that irisin exerts protection via AMPK/PGC-1α pathway activation and SIRT3 acts downstream of PGC-1α , we hypothesized mediates irisin's neuroprotection CIR In vivo was modeled by inducing transient middle artery occlusion (MCAO) mice, while vitro conditions were replicated using oxygen-glucose deprivation (OGD) PC12 neuronal cultures. To elucidate the mechanistic role targeted interventions implemented: expression silenced transfection with small interfering RNA (siRNA), its enzymatic activity pharmacologically inhibited 3-TYP, selective inhibitor. Apoptotic systematically evaluated through TUNEL staining, Western blot analysis caspase-3, Bax Bcl-2. Oxidative stress parameters, including malondialdehyde (MDA) levels glutathione (GSH) content, measured colorimetric assays. Neurological function mice quantified modified Severity Score (mNSS). Our results demonstrated mitigates apoptosis oxidative dose-dependently activating signaling. At optimal dosage, effectively restored levels, reduced damage, improved neurological recovery models. Notably, significantly attenuated specific Further validation experiments revealed overexpression synergistically enhanced irisin-mediated OGD-induced injury, whereas knockout substantially diminished efficacy. data shown exerted protective at least part, activation. This study establishes irisin/SIRT3 as novel target for ischemic stroke, providing insights future interventions.
Язык: Английский
Процитировано
0Biomolecules, Год журнала: 2024, Номер 14(8), С. 973 - 973
Опубликована: Авг. 9, 2024
The kidney performs fundamental functions by eliminating metabolic waste and reabsorbing essential nutrients electrolytes such as glucose, proteins, ions, anions [...].
Язык: Английский
Процитировано
1Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2024, Номер unknown
Опубликована: Ноя. 23, 2024
Abstract Nonsteroidal anti-inflammatory drug (NSAID)-induced kidney injury is one of the most common causes renal failure. The exact pathogenesis NSAID induced not fully known and treatment still challenging. Artemisinin (ART) gains more attention by its potent biological activities in addition to antimalarial effect. In our research, we evaluated preventive therapeutic effects ART Diclofenac (DIC) through effect on mitochondria regulation sirtuin 3 (SIRT3). Thirty adult male Sprague Dawley rats were divided into five groups: control, ART, DIC, DIC + prophylactic, followed groups. At end study, animals scarified following parameters evaluated: serum urea creatinine, malondialdehyde (MDA), superoxide dismutase (SOD) nitrate. SIRT3 was detected western blotting real-time PCR. Mitochondrial related markers (PGC-1α, Drp1, mitochondrial ATP) immunoassay. Caspase-3 LC3 II expression tissues demonstrated immune-histochemical staining. specimens stained for H&E PAS special stain. Electron microscopy done detect morphology. improved function test, oxidative stress, level, function, decrease caspase-3. Histopathological examination confirmed alleviation as determined light or electron microscopy. can modulate biochemical pathological changes DIC-induced be considered a new possible approach SIR3 maintenance homeostasis.
Язык: Английский
Процитировано
0Bioorganic & Medicinal Chemistry, Год журнала: 2024, Номер unknown, С. 118045 - 118045
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
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