Neuroprotectant Effects of Hibiscetin in 3-Nitropropionic Acid-Induced Huntington's Disease via Subsiding Oxidative Stress and Modulating Monoamine Neurotransmitters in Rats Brain

• Published in: Molecules (Basel, Switzerland) Vol. 28; no. 3; p. 1402
• Main Authors: Mahdi, Wael A, AlGhamdi, Shareefa A, Alghamdi, Amira M, Imam, Syed Sarim, Alshehri, Sultan, Almaniea, Mohammad A, Hajjar, Baraa Mohammed, Al-Abbasi, Fahad A, Sayyed, Nadeem, Kazmi, Imran
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.02.2023; MDPI
• Subjects: 3-Nitropropionic acid; Acute toxicity; Animal cognition; Animal models; Animals; Body Weight; Brain; Brain research; Brain-derived neurotrophic factor; Care and treatment; Caspase-3; Disease; Dopamine; Evaluation; Flavonoids; Health aspects; hibiscetin; Huntington Disease - chemically induced; Huntington Disease - drug therapy; Huntington's chorea; Huntington's disease; Huntingtons disease; Inflammation; Monoamines; Neurodegeneration; Neurons; Neuroprotection; Neuroprotective agents; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Neurotransmitter Agents - pharmacology; Neurotransmitters; Nitro Compounds - pharmacology; Norepinephrine; Oxidative Stress; Peroxidase; Pharmacology, Experimental; Physiological effects; Phytochemicals; Propionates - pharmacology; Proteins; Rats; Rats, Wistar; Serotonin; Signs and symptoms; Toxicity; Tumor necrosis factor-TNF; Tumor necrosis factor-α; γ-Aminobutyric acid; Saudi Arabia; Huntington’s disease; 3-nitropropionic acid; hibiscetin; neuroprotection
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules28031402

Previously reported data suggest that hibiscetin, isolated from , contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD). To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups ( = 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1β), and myeloperoxidase (MPO) were evaluated. The hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin. The current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models.