Anti-Huntington's Effect of Rosiridin via Oxidative Stress/AchE Inhibition and Modulation of Succinate Dehydrogenase, Nitrite, and BDNF Levels against 3-Nitropropionic Acid in Rodents

• Published in: Biomolecules (Basel, Switzerland) Switzerland), 2022-07, Vol.12 (8), p.1023
• Main Authors: Afzal, Muhammad, Sayyed, Nadeem, Alharbi, Khalid Saad, Alzarea, Sami I, Alshammari, Mohammed Salem, Alomar, Fadhel A, Alenezi, Sattam Khulaif, Quazi, Anwarulabedin Mohsin, Alzarea, Abdulaziz I, Kazmi, Imran
• Format: Article
• Language: English
• Subjects: 3-Nitropropionic acid; Acetylcholinesterase; Acids; Acute toxicity; Analysis; Animal models; Animals; Brain research; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - blood; Care and treatment; Catalase; Central nervous system; Chemicals; Cognitive ability; Dehydrogenases; Diagnosis; Disease control; Drug dosages; Glutathione; Health aspects; Huntington Disease; Huntington's chorea; Huntington's disease; Huntingtons disease; Inflammation; Laboratories; Latency; Materia medica, Vegetable; Measurement; Methods; Motor Activity; Mutation; Neurodegeneration; Neurophysiology; neuroprotection; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Nitrites - metabolism; Nitro Compounds; Oxidative Stress; Plant extracts; Propionates; Proteins; Rats; Rats, Wistar; Risk factors; rosiridin; Succinate dehydrogenase; Succinate Dehydrogenase - metabolism; TNF-α; Toxicity
• ISSN: 2218-273X; 2218-273X
• DOI: 10.3390/biom12081023

Rosiridin is a compound extracted from ; water extracts of root elicit positive effects on the human central nervous system and improve brain function. They are also thought to be beneficial to one's health, in addition to being antioxidants. The present study aims to evaluate the anti-Huntington's effect of rosiridin against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD)-like effects in rats. The acute toxicity in rats was elucidated to track the conceivable toxicities in the rats. The effectiveness of rosiridin at a dosage of 10 mg/kg was evaluated against several dose administrations of 3-NPA-induced HD-like symptoms in the rats for 22 days. At the end of the study, behavioral parameters were assessed as a hallmark for the cognitive and motor functions in the rats. Similarly, after the behavioral assessment, the animals were sacrificed to obtain a brain tissue homogenate. The prepared homogenate was utilized for the estimation of several biochemical parameters, including oxidative stress (glutathione, catalase, and malondialdehyde), brain-derived neurotrophic factor and succinate dehydrogenase activity, and the glutamate and acetylcholinesterase levels in the brain. Furthermore, inflammatory mediators linked to the occurrence of neuroinflammation in rats were evaluated in the perfused brain tissues. The rosiridin-treated group exhibited a significant restoration of behavioral parameters, including in the beam-walk test, latency in falling during the hanging wire test, and percentage of memory retention during the elevated plus-maze test. Further, rosiridin modulated several biochemical parameters, including oxidative stress, pro-inflammatory activity, brain-derived neurotrophic factor, nitrite, and acetylcholinesterase as compared to disease control group that was treated with 3-NPA. The current study exhibits the anti-Huntington's effects of rosiridin in experimental animal models.