<i>Sarcocephalus latifolius</i> Ethanol Leaf Extract Attenuates Rotenone-Induced Behavioural Deficits, Oxidative Stress and Neuroinflammation in a Rat Model of Parkinsonism
DOI:
https://doi.org/10.51412/psnnjp.2026.016Keywords:
Sarcocephalus latifolius ethanol extract (SLEE), Rotenone, Oxidative stress, Parkinson's diseaseAbstract
Background and Aim: Sarcocephalus latifolius (Sm.) E.A. Bruce is a medicinal plant with recognized antimicrobial, antioxidant, anti-inflammatory, and antidiabetic properties. This study evaluated the protective effects of Sarcocephalus latifolius ethanol leaf extract (SLEE) against rotenone-induced neurotoxicity, oxidative stress, and neuroinflammation in rat brain regions.
Materials and methods: Male Wistar rats were divided into four groups (n = 5). Group 1 received control treatment (1% ethanol in sunflower oil, i.p.) for 28 days, while group 2 was administered rotenone (2.5 mg/kg, i.p.) on 14 alternate days during the 28-day experimental period. Group 3 received SLEE (400 mg/kg, p.o.) alongside rotenone (2.5 mg/kg, i.p.), and group 4 received Levodopa/Carbidopa (25 mg/kg, p.o.) plus rotenone (2.5 mg/kg, i.p.) for 28 days. Behavioural assessments including catalepsy, negative geotaxis, Y-maze, elevated plus maze, and sucrose splash tests were conducted on day 29. Biochemical assessments of MDA, nitrite, GSH, SOD, GST, proinflammatory cytokines (TNF-α and IL-6), AChE activity, and dopamine concentration were performed in the prefrontal cortex (PFC), striatum (STR), cerebellum (CER), and hippocampus (HPC).
Results: Rotenone significantly increased catalepsy duration, negative geotaxis latency, oxidative stress markers (MDA and nitrite), AChE activity, and pro-inflammatory cytokines (TNF-α and IL-6), while reducing Y-maze alternation, grooming duration, antioxidant status (GSH, SOD, GST, and CAT), and dopamine levels compared with vehicle controls (p < 0.05). It also impaired elevated plus maze performance by reducing open arm exploration (p < 0.05). SLEE treatment significantly improved negative geotaxis performance [F(3,16)=39.10, p<0.0001] and spontaneous alternation [F(3,16)=37.98, p<0.0001] compared with rotenone-treated rats, although effects on catalepsy, grooming duration and open arm behaviour were not significant. SLEE significantly attenuated rotenone-induced alterations compared with the rotenone group, with significant treatment effects observed for oxidative stress markers (p<0.05), dopamine concentration [F(3,48)=497.3, p<0.0001], AChE activity [F(3,64)=43.10, p<0.0001], TNF-α [F(3,48)=124.7, p<0.0001], and IL-6 [F(3,48)=50.53, p<0.0001].
Conclusion: SLEE treatment demonstrated a potential to reverse oxidative stress and modulate neuroinflammation induced by rotenone. These effects on antioxidant enzyme activities and proinflammatory cytokines suggest that SLEE may offer ameliorative benefits in neurodegenerative conditions.
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