Tinospora cordifolia Suppresses Neuroinflammation in Parkinsonian Mouse Model

• DOI: 10.1007/s12017-018-08521-7
• Publication Date: 2019-01-14T11:12:01Z
• Authors: Hareram Birla; Sachchida Nand Rai; Saumitra Sen Singh; Walia Zahra; Arun Rawat; Neeraj Tiwari; Rakesh K. Singh; Abhishek Pathak; Surya Pratap Singh
• Keywords: Male; 0301 basic medicine; 0303 health sciences; Dose-Response Relationship, Drug; Dopaminergic Neurons; Anti-Inflammatory Agents; MPTP Poisoning; Nerve Tissue Proteins; Corpus Striatum; Medicine, Ayurvedic; 3. Good health; Mice, Inbred C57BL; Disease Models, Animal; Mice; Oxidative Stress; 03 medical and health sciences; Neuroprotective Agents; Gene Expression Regulation; Parkinsonian Disorders; Astrocytes; Animals; Cytokines; Lipid Peroxidation; Microglia

Parkinson's disease (PD), a neurodegenerative central nervous system disorder, is characterised by progressive loss of nigrostriatal neurons in basal ganglia. Previous studies regarding PD have suggested the role of oxidative stress along with neuroinflammation in neurodegeneration. Accordingly, our study explore the anti-inflammatory activity of Tinospora cordifolia aqueous extract (TCAE) in 1-methyl-4-phenyl-1,2,3,6-tetra hydropyridine (MPTP)-intoxicated Parkinsonian mouse model. MPTP-intoxicated mice showed significant behavioral and biochemical abnormalities which were effectively reversed by TCAE. It is evident that TCAE inhibits the MPTP-intoxicated Nuclear factor-κB (NF-κB) activation and its associated pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) from immunohistochemistry and Western blot analysis. In MPTP-intoxicated mice, microglial and astroglial-specific inflammatory markers, ionized calcium binding adaptor molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP), respectively were increased while were significantly reduced in TCAE treatment. Expression of pro-inflammatory cytokine genes, TNF-α, Interleukin-12 (IL-12) and Interleukin-1β (IL-1β) were found to be upregulated in MPTP-intoxicated mice, whereas TCAE treatment restored their levels. Additionally, anti-inflammatory factor Interleukin-10 (IL-10) gene was found to be downregulated in MPTP-intoxicated mice which were significantly restored by TCAE treatment. Tyrosine hydroxylase (TH) expression was reduced in MPTP-intoxicated mice, while its expression was significantly increased in TCAE-treated group. Our result strongly suggests that T. cordifolia protects dopaminergic neurons by suppressing neuroinflammation in MPTP-induced Parkinsonian mouse model.