A Novel Pharmacological Protective Role for Safranal in an Animal Model of Huntington’s Disease

Fotoohi, Ahmad; Moloudi, Mohammad Raman; Hosseini, Saed; Hassanzadeh, Kambiz; Feligioni, Marco; Izadpanah, Esmael

doi:10.1007/s11064-021-03271-8

Cited by 16 publications

(13 citation statements)

References 23 publications

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“…There are various known therapeutic extracts obtained from saffron, including crocetin, crocin, picrocrocin, and safranal . Safranal, which belongs to the monoterpene aldehyde family, has effects similar to those of saffron, particularly in terms of cardiovascular disease treatment, alleviating asthma, Huntington’s disease treatment, neurodegenerative retinal diseases treatment, and so on. In addition, safranal has been reported in many research works about regulating immune functions; the effect on immune system deserves furtherly studying.…”

Section: Discussionmentioning

confidence: 99%

Safranal Treatment Induces Sirt1 Expression and Inhibits Endoplasmic Reticulum Stress in Mouse Chondrocytes and Alleviates Osteoarthritis Progression in a Mouse Model

Zhang

Chen

et al. 2022

J. Agric. Food Chem.

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Osteoarthritis (OA) is an age-related degenerative disease. Oxidative stress (OS) modulates OA pathogenesis by enhancing chondrocyte apoptosis and extracellular matrix (ECM) degeneration via activation of the endoplasmic reticulum (ER) stress. Prior studies revealed that safranal plays a critical role in multiple diseases treatments, but there are no reports on its effect on OA. Therefore, investigating the effect of safranal on OA is needed. As a compound that can lead excessive reactive oxygen species (ROS) accumulation, tert-butyl hydroperoxide (TBHP) was used to induce OS and OS-mediated endoplasmic reticulum (ER) stress for imitating OA in vitro. Besides, the bilateral medial meniscus was removed to induce joint instability and excessive friction of the joint surface to establish destabilization of medial meniscus for imitating the initiation and progression of OA in vivo. We, next, conducted Western blot and RT-PCR analyses to identify biomarkers of the underlying signaling pathway. Our results demonstrated that 30 μM safranal strongly upregulated Sirt1 expression, suppressed TBHP-mediated ER stress, and, in turn, prevented chondrocyte apoptosis and ECM degeneration. Furthermore, compared with the other two classic signaling pathways of ER stress, safranal can inhibit the PERK-eIF2α-CHOP axis at the lower concentration (5 and 15 μM). In vivo, using Safranin O staining, X-ray, immunofluorescence (IF), and immunohistochemical (IHC) staining, we demonstrated that OA progression can be postponed with intraperitoneal injection of 90 and 180 mg/kg safranal in an OA mouse model. Taken together, our analyses revealed that safranal can potentially prevent OA development.

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Section: Discussionmentioning

confidence: 99%

Safranal Treatment Induces Sirt1 Expression and Inhibits Endoplasmic Reticulum Stress in Mouse Chondrocytes and Alleviates Osteoarthritis Progression in a Mouse Model

Zhang

Chen

et al. 2022

J. Agric. Food Chem.

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“…Previously, we obtained a similar pattern in locomotor activity, body weight, and biochemical parameters following 3-NP injection in rats (Fotoohi, 2021). 3-Nitropropionic acid is gaining attention as a valuable tool to mimic behavioral, biochemical, and morphologic changes similar to those occurring in HD [18].…”

Section: Discussionmentioning

confidence: 74%

Alpha-Pinene Alleviates Motor Activity in Animal Model of Huntington’s Disease via Enhancing Antioxidant Capacity

et al. 2023

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Huntington's disease is a progressive, neurodegenerative, and inherited disease. Antioxidants have been shown effective in slowing disease progression in animal models of HD and are under investigation in human clinical trials. α-Pinene, a polyphenolic compound of the terpene family, has been shown to exert antioxidant activity. Therefore, this study aimed to investigate the impact of α-pinene on animal model of HD.Thirty-two male Wistar rats received 3-Nitropropionic acid (3-NP) for induction of the disease model or treated with α-pinene + 3-NP in different groups. Motor skill, and biochemical evaluations to detect oxidant/antioxidant markers in rat cortex and striatum were performed in all groups. We found that αpinene signi cantly improved 3-NP-induced changes in the body weight, rotarod activity, time taken to cross the narrow beam, and locomotor activity. Biochemical analysis revealed that α-pinene signi cantly decreased the 3NP-induced elevation in oxidant markers, nitrite, and malondialdehyde in both cortex and striatum. In addition, α-pinene counteracted the 3NP-induced fall in antioxidant enzymes, including superoxide dismutase, catalase, and glutathione in the cortex and striatum.In conclusion, we found that α-pinene prevented the motor dysfunction induced by 3-NP in the animal model of Huntington's disease. Oxidants-antioxidant balance might be involved in the protective effect of α-pinene.

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“…Europinidin may protect mitochondrial integrity by maintaining the activity of mitochondrial enzyme complexes, particularly complexes I, II, and IV. This preservation of mitochondrial function could help sustain cellular energy production and minimize oxidative damage [ 15 , 16 , 17 , 18 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

“…The herbaceous species Ceratostigma plumbaginoides and Plumbago europea, which produce the o-methylated derivative of delphinidin known as europinidin, are members of the Plumbaginaceae family. Plumbago europea , a perineal herb, is used to treat a diverse range of illnesses including cancer, immunosuppression, dysmenorrhea, hepatitis, respiratory problems, edema, and scabies [ 13 , 14 , 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

Alharbi

2024

Biomedicines

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Huntington’s disease (HD) is a neurodegenerative disease that causes progressive motor and cognitive dysfunction. There is no cure for HD, and current therapeutics can only manage the signs and symptoms as well as slowing disease progression. This investigation examines the possible therapeutic advantages of europinidin in 3-nitropropionic acid (3-NPA) injected HD in rats. Wistar rats were randomly assigned to five groups (n = 6): normal control, 3-NPA (10 mg/kg, i.p.), 3-NPA + europinidin-10 (10 mg/kg, p.o.), 3-NPA + europinidin-20 (20 mg/kg, p.o.), and europinidin alone (20 mg/kg, p.o.) for 15-day. Various behavioral and biochemical parameters including antioxidant levels, oxidative stress, pro-inflammatory markers, mitochondrial enzyme complex, and neurotransmitters were assessed. Europinidin restored biochemical, mitochondrial dysfunction, oxidative stress, neurotransmitter, and pro-inflammatory parameters disrupted by 3-NPA. Here we show that europinidin attenuates 3-NPA-induced neurodegeneration in rat models of HD. Europinidin modulates oxidative stress, enhances antioxidants, restores mitochondrial enzyme complex activity, reduces neuroinflammation, and modulates neurotransmitter levels. Our findings reveal the potential of europinidin as a novel therapeutic agent for the treatment of HD. This study also provides new insights into the molecular mechanisms of europinidin-mediated neuroprotection and may have a beneficial role in the management of neurological diseases.

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A Novel Pharmacological Protective Role for Safranal in an Animal Model of Huntington’s Disease

Cited by 16 publications

References 23 publications

Safranal Treatment Induces Sirt1 Expression and Inhibits Endoplasmic Reticulum Stress in Mouse Chondrocytes and Alleviates Osteoarthritis Progression in a Mouse Model

Safranal Treatment Induces Sirt1 Expression and Inhibits Endoplasmic Reticulum Stress in Mouse Chondrocytes and Alleviates Osteoarthritis Progression in a Mouse Model

Alpha-Pinene Alleviates Motor Activity in Animal Model of Huntington’s Disease via Enhancing Antioxidant Capacity

Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations

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