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

Abstract

Background: Rosiridin is a compound extracted from Rhodiola sachalinensis; water extracts of Rhodiola 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. Materials and Methods: 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. Results: 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. Conclusions: The current study exhibits the anti-Huntington’s effects of rosiridin in experimental animal models.

Rosiridin Attenuates Scopolamine-Induced Cognitive Impairments in Rats via Inhibition of Oxidative and Nitrative Stress Leaded Caspase-3/9 and TNF-α Signaling Pathways

“…According to previously published research, monoamine oxidase (MAO) activation has a crucial role in the pathogenesis of AD, including the creation of amyloid plaques from Aβ production. Rosiridin can be used to treat early-onset dementia and despair because it inhibits monoamine oxidase A and B [39]. Rosiridin has recently been found to have an anti-Huntington's effect through oxidative stress/acetylcholine esterase (AChE), and inhibition and modulation of succinate dehydrogenase, nitrite, and brain-derived neurotrophic factor levels against 3-nitropropionic acid in rodents [39].…”

“…Rosiridin can be used to treat early-onset dementia and despair because it inhibits monoamine oxidase A and B [39]. Rosiridin has recently been found to have an anti-Huntington's effect through oxidative stress/acetylcholine esterase (AChE), and inhibition and modulation of succinate dehydrogenase, nitrite, and brain-derived neurotrophic factor levels against 3-nitropropionic acid in rodents [39]. However, no research has been completed on the impact of rosiridin on cognitive impairment caused by scopolamine.…”

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

“…Before start of study, the rats from all groups were subjected to a seven-day acclimatization period under controlled laboratory conditions. To induce prompt toxicity in rodents, 3-NPA in saline (pH 7.4) will be administered once daily for 15 days based on previously conducted protocols [ 65 , 66 , 67 ]. In the current investigation, animals were allocated to four groups ( n = 6).…”

Rosinidin Protects Streptozotocin-Induced Memory Impairment-Activated Neurotoxicity by Suppressing Oxidative Stress and Inflammatory Mediators in Rats

“…The study followed OECD Guideline Acute Toxicity Study No. 423 [ 24 , 25 ]. The test drug was orally administered to the rats at the maximum dose.…”