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Potential ameliorative effect ofCynodon dactylon (L.) pers on scopolamine‑induced amnesia in rats: Restoration of cholinergic and antioxidant pathways

By: Contributor(s): Publication details: Mumbai Wolter Kluwer 2021Edition: Vol.53(1), Jan-FebDescription: 50-59pSubject(s): Online resources: In: Indian Journal of PharmacologySummary: AIM: The present study explored Cynodon dactylon hydro‑ethanolic extract (CDE) effect on scopolamine‑induced amnesic rats. MATERIALS AND METHODS: C. dactylon extract was subjected to antioxidant (DPPH and H2O2) and acetylcholinesterase enzyme tests by in vitro methods. Scopolamine (1 mg/kg, i.p) was administered to rats except for normal control. Donepezil (3 mg/kg, p.o), CDE (100, 200, and 400 mg/kg p.o) were administered to treatment groups. Behavioral paradigm: Morris water maze (MWM), elevated plus maze (EPM), and passive avoidance test (PAT) were conducted. Later, rats were sacrificed and brain homogenate was tested for levels of acetylcholinesterase, glutathione, and lipid peroxidase. Histopathology examination of cortex and hippocampus of all the groups was done. STATISTICAL METHOD: The statistical methods used were ANOVA and Tukey’s post hoc test. RESULTS: CDE antioxidant activity was demonstrated by decreasing DPPH and H 2O2 levels confirmed through in vitro analysis. Treatment group rats reversed scopolamine induced amnesia by improvement in spatial memory, decreased transfer latency and increased step through latency significantly (P<0.001) in behavior models such as morris water maze, elevated plus maze and passive avoidance task respectively. CDE modulated acetylcholine transmission by decreased acetylcholinesterase enzyme level (P < 0.001) and scavenging scopolamine‑induced oxidative stress by increased reduced glutathione levels and decreased lipid peroxidation levels in the rat brain. CDE and donepezil‑treated rats showed mild neurodegeneration in comparison to scopolamine‑induced severe neuronal damage on histopathology examination. CONCLUSION: C. dactylon extract provides evidence of anti‑amnesic activity by the mechanism of decreased acetylcholinesterase enzyme level and increased antioxidant levels in scopolamine‑induced amnesia in rats.
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AIM: The present study explored Cynodon dactylon hydro‑ethanolic extract (CDE) effect on
scopolamine‑induced amnesic rats.
MATERIALS AND METHODS: C. dactylon extract was subjected to antioxidant (DPPH and H2O2) and
acetylcholinesterase enzyme tests by in vitro methods. Scopolamine (1 mg/kg, i.p) was administered
to rats except for normal control. Donepezil (3 mg/kg, p.o), CDE (100, 200, and 400 mg/kg p.o) were
administered to treatment groups. Behavioral paradigm: Morris water maze (MWM), elevated plus
maze (EPM), and passive avoidance test (PAT) were conducted. Later, rats were sacrificed and
brain homogenate was tested for levels of acetylcholinesterase, glutathione, and lipid peroxidase.
Histopathology examination of cortex and hippocampus of all the groups was done.
STATISTICAL METHOD: The statistical methods used were ANOVA and Tukey’s post hoc test.
RESULTS: CDE antioxidant activity was demonstrated by decreasing DPPH and H 2O2 levels
confirmed through in vitro analysis. Treatment group rats reversed scopolamine induced amnesia
by improvement in spatial memory, decreased transfer latency and increased step through latency
significantly (P<0.001) in behavior models such as morris water maze, elevated plus maze and
passive avoidance task respectively. CDE modulated acetylcholine transmission by decreased
acetylcholinesterase enzyme level (P < 0.001) and scavenging scopolamine‑induced oxidative stress
by increased reduced glutathione levels and decreased lipid peroxidation levels in the rat brain. CDE
and donepezil‑treated rats showed mild neurodegeneration in comparison to scopolamine‑induced
severe neuronal damage on histopathology examination.
CONCLUSION: C. dactylon extract provides evidence of anti‑amnesic activity by the mechanism of
decreased acetylcholinesterase enzyme level and increased antioxidant levels in scopolamine‑induced
amnesia in rats.

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