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SCIENTIFIC LITERATURE · MED

⁇ i>Tinospora sinensis ⁇ /i> nöroprotektif sırlarını çözme: Parkinson hastalığı sıçan modellerinde davranışsal ve biyokimyasal zorlukların rotenone indüklenmiş fırtınasında gezinmek.

Decoding the neuroprotective secrets of <i>Tinospora sinensis</i>: navigating the rotenone induced storm of behavioral and biochemical challenges in Parkinson's disease rat models.

Makine çevirisi · Editoryal inceleme bekliyor

J Complement Integr Med · 2026-06-09

DOI: 10.1515/jcim-2026-0074PMID: 42287110

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ObjectivesParkinson's disease (PD) is a chronic neurodegenerative disorder that leads to motor and non-motor challenges, significantly impacting the quality of life. Research highlights body's antioxidant systems role in mitigating PD. This study investigated neuroprotective capabilities of Tinospora sinensis stem extract (TSSE) in a rat model of PD induced by rotenone.MethodsPD was induced in rats by subcutaneous rotenone injections (2 mg/kg/day) for 35 days. TSSE was administered orally at 100, 200, and 400 mg/kg doses, with levodopa-carbidopa as the standard reference. Motor impairments were assessed through catalepsy, locomotor activity, and rotarod tests. Biochemical evaluations included oxidative stress markers, antioxidant enzymes (glutathione, superoxide dismutase, and catalase), and dopamine levels, and monoamino oxidase-B (MAO-B). Histopathological examination of brain assessed neuronal integrity.ResultsRotenone administration led to significant motor impairments, increased oxidative stress, reduced dopamine levels, and neuronal damage. Treatment with TSSE resulted in notable, dose-dependent enhancements in motor abilities and restored antioxidant enzyme activities, while also reducing lipid peroxidation, as indicated by decreased malondialdehyde levels. Additionally, TSSE decreased MAO-B level and increased brain dopamine level and maintained neuronal structure. The TSSE 400 mg/kg exhibited neuroprotective effects comparable to those of standard.ConclusionsTSSE shows significant neuroprotective effects, likely by enhancing endogenous antioxidant defenses and restoring dopaminergic neurotransmission. These findings suggest, TSSE could serve as a complementary therapeutic approach that targets oxidative and neurodegenerative mechanisms in PD.

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