Pharmacological Assessment of Aqueous Ethanolic Extract of Thalictrum Foetidum Against Haloperidol-Induced Parkinson’s Like Symptoms in Animal Model: A Dose-Dependent Study With Mechanistic Approach

Author:

Han Jiangyu1,Hao Xu2,Fatima Mishal3,Chauhdary Zunera3,Jamshed Ayesha4,Abdur Rahman Hafiz Muhammad5,Siddique Rida3,Asif Muhammad3,Rana Saba3ORCID,Hussain Liaqat3ORCID

Affiliation:

1. School of Medicine, Huzhou University, Huzhou, P.R China

2. College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou, P.R China

3. Department of Pharmacology, Faculty of Pharmaceutical Sciences, Government College University Faisalabad, Faisalabad, Pakistan

4. Department of Pharmacology, Faculty of Pharmacy, The Islamia University of Bahawalpur, Bahawalpur, Pakistan

5. Pharmacology Section, Department of Pharmacy, Institute of Southern Punjab Multan, Multan, Pakistan

Abstract

Introduction: Parkinson’s disease (PD) is characterized by dopamine deficiency in the corpus striatum due to the degeneration of dopaminergic neurons in the substantia nigra. Symptoms include bradykinesia, resting tremors, unstable posture, muscular rigidity, and a shuffled gait. Thalictrum foetidum is traditionally used for neurodegenerative disorders. Objectives: This study aimed to explore the therapeutic potential of aqueous ethanolic extract of Thalictrum foetidum (AETF) against Parkinson-like symptoms and to investigate its underlying mechanism. Methodology: Thirty-six albino mice were randomly divided into 6 groups (n = 6): normal control, disease control, standard treatment (levodopa/carbidopa, 100/25 mg/kg), and 3 treatment groups (AETF at 200, 400, and 600 mg/kg). One hour before treatment, haloperidol (1 mg/kg, i. p.) was administered to induce Parkinson’s disease in all groups except the normal control group. Results: Behavioral analysis showed significant improvement ( P < .001) in motor function, muscular coordination, and reduced muscular rigidity and tremors. AETF also reduced oxidative stress. Histological examination of the brain showed reduced Lewy bodies, neurofibrillary tangles, and plaque formation. Conclusion: AETF alleviated PD symptoms by reducing neurodegeneration, modulating oxidative stress, and inhibiting the expression of nuclear factor-κB (NF-κB) and associated inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6).

Publisher

SAGE Publications

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