Pharmacological Characterization of Ruellia tuberosa Ethanolic Extract in a Rodent Model of Cognitive Impairment.

Introduction: Cognitive impairment linked to neurodegenerative diseases poses a considerable challenge, requiring the exploration of plant-derived therapeutic alternatives. Ruellia tuberosa, a medicinal plant recognized for its anti-oxidant and anti-inflammatory properties, was examined for its therapeutic potential in a rodent model of memory impairment.

Method: The present study aimed to evaluate the effects of Ruellia tuberosa ethanolic extract (RTEE) on aluminium chloride (AlCl3)-induced Alzheimer's disease (AD) in adult Wistar rats. In-vitro cell line study showed decreased formation of reactive oxygen species (ROS), decreased levels of IL-6 (Interleukin-6), and suppressed NF-κB (Nuclear factor kappa-B) translocation, which further confirmed RTEE's antioxidant and anti-inflammatory characteristics. Following the objective, thirty adult Wistar rats were taken and divided into five groups (n=6). They were treated with Normal saline, AlCl3 (100 mg/kg), DPZ (Donepezil- 3 mg/kg), and RTEE (100 and 200 mg/kg), respectively, for 35 days.

Results: Various behavioral and biochemical parameters, along with the oxidative and inflammatory biomarkers, were assessed to determine the effects of RTEE. The plant extract at both the doses (100 and 200 mg/kg) demonstrated increased body weight, improved motor coordination as demonstrated by an increase in fall-off time on the Rota rod apparatus, decreased escape latency in the Morris water maze test, reduced transfer latency (TL) in the elevated plus maze test, increased time spent in the target quadrant, and increased exploration time in the novel object recognition test. Furthermore, RTEE treatment exhibited decreased levels of malondialdehyde (MDA) and acetylcholinesterase (AChE) activity and increased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and total protein. Additionally, RTEE reduced levels of inflammatory cytokines, such as TNF-α and IL-1β, which decreased neuroinflammation and amyloid-beta levels. Additionally, the extract exhibited cholinergic system modulation, as observed by improved acetylcholinesterase activity, suggesting its potential role in neurotransmitter regulation. Histopathological study further confirmed its neuroprotective potential by reducing neuronal degeneration in brain regions (hippocampus and cortex).

Conclusion: According to the study's findings, memory impairment in the AlCl3-induced rat model of AD was ameliorated by both doses of RTEE. However, further studies need to be conducted to establish its therapeutic effects in neurodegenerative diseases.