Protective role of apigenin on rotenone induced rat model of Parkinson's disease: Suppression of neuroinflammation and oxidative stress mediated apoptosis

Anusha, Chandran; Sumathi, Thangarajan; Joseph, Leena Dennis

doi:10.1016/j.cbi.2017.03.016

Cited by 152 publications

(74 citation statements)

References 112 publications

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“…Additionally, an inflammatory response develops within several hours after damage and is characterized by the activation of pro-inflammatory cytokines and infiltration of neutrophils (Fu et al, 2018). The inflammatory response makes neurological injury in a worse situation and promotes neural cells apoptosis (Anusha et al, 2017). A large number of evidences showed that the pro-inflammatory cytokines released in the periphery and neuronal apoptosis induced by cerebral I/R may occur potential injury to the hippocampal cells, which are associated with memory and learning functions (Chen et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

et al. 2020

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The aim of this research is to investigate the potential neuro-protective effect of kaempferol which with anti-oxidant, anti-inflammatory, and immune modulatory properties, and understand the effect of kaempferol on reducing cerebral ischemia reperfusion (I/R) injury in vivo. Male adult Sprague Dawley (SD) rats were pretreated with kaempferol for one week via gavage before cerebral I/R injury operation. We found that kaempferol treatment can reduce the cerebral infarct volume and neurological score after cerebral I/R. Rats were sacrificed after 24 h reperfusion. We observed that kaempferol improved the arrangement, distribution, and morphological structure of neurons, as well as attenuated cell apoptosis in brain tissue via hematoxylin and eosin (H&E) staining, Nissl staining and TUNEL staining. Superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH) kit analysis, enzyme-linked immunosorbent (ELISA) assay, real-time PCR, Western blot, and immunohistochemical examination indicated that kaempferol mitigated oxidative and inflammatory stress via regulating the expression of proteins, p-Akt, p-GSK-3b, nuclear factor erythroid2-related factor 2 (Nrf-2), and p-NF-kB during cerebral I/R, thus increasing the activity of SOD and GSH, meanwhile decreasing the content of MDA in serum and brain tissue, as well as restoring the expression levels of tumor necrosis factor alpha (TNF-a), interleukin-1b (IL-1b), and IL-6 in vivo. Taken together, this study suggested that kaempferol protects against cerebral I/R induced brain damage. The possible mechanism is related with inhibiting oxidative and inflammatory stress induced apoptosis.

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Section: Discussionmentioning

confidence: 99%

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

et al. 2020

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“…Aminothiazoles derivatives as SUMOylation activators [124] AMN082 [115] Amodiaquine [125,126] Antagonist of the A(2A) adenosine receptor-derivative 49 [127] Apigenin [128][129][130][131] Apomorphine [132,133] l-Arginine [134] Aromadendrin [128] Ascorbic acid [135,136] ASI-1 [12] ASI-5 [12] Astilbin [137] Azilsartan [138] Baicalein [139][140][141] Benserazide [142,143] 7H-Benzo, perimidin-7-one derivatives (R6 = OH) [144] 4H-1-Benzopyran-4-one [145] 8-Benzyl-tetrahydropyrazino, purinedione derivatives (derivative n.57) [146] Bikaverin [147]…”

Section: Compound Name(s) Referencesmentioning

confidence: 99%

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

Tosato

Marco

2019

Biomolecules

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The present review reports a list of approximately 800 compounds which have been used, tested or proposed for Parkinson’s disease (PD) therapy in the year range 2014–2019 (April): name(s), chemical structure and references are given. Among these compounds, approximately 250 have possible or established metal-chelating properties towards Cu(II), Cu(I), Fe(III), Fe(II), Mn(II), and Zn(II), which are considered to be involved in metal dyshomeostasis during PD. Speciation information regarding the complexes formed by these ions and the 250 compounds has been collected or, if not experimentally available, has been estimated from similar molecules. Stoichiometries and stability constants of the complexes have been reported; values of the cologarithm of the concentration of free metal ion at equilibrium (pM), and of the dissociation constant Kd (both computed at pH = 7.4 and at total metal and ligand concentrations of 10–6 and 10–5 mol/L, respectively), charge and stoichiometry of the most abundant metal–ligand complexes existing at physiological conditions, have been obtained. A rigorous definition of the reported amounts is given, the possible usefulness of this data is described, and the need to characterize the metal–ligand speciation of PD drugs is underlined.

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“…These effects are related to the inhibition of NF-κB-dependent pro-inflammatory cytokines [33], VEGF, ICAM-1, STAT3 [34], and activation of antioxidant transcription factor Nrf2 [33]. Many flavonoids, as apigenin and vitexin, were reported to be safe natural alternative therapeutic against neuroinflammatory diseases as such Multiple Sclerosis (MS) [35,36]. Therefore, flavonoids are multi-target drugs, which explain their wide array of actions.…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Potential of Flavonoids in Pain and Inflammation: Mechanisms of Action, Pre-Clinical and Clinical Data, and Pharmaceutical Development

et al. 2020

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Pathological pain can be initiated after inflammation and/or peripheral nerve injury. It is a consequence of the pathological functioning of the nervous system rather than only a symptom. In fact, pain is a significant social, health, and economic burden worldwide. Flavonoids are plant derivative compounds easily found in several fruits and vegetables and consumed in the daily food intake. Flavonoids vary in terms of classes, and while structurally unique, they share a basic structure formed by three rings, known as the flavan nucleus. Structural differences can be found in the pattern of substitution in one of these rings. The hydroxyl group (-OH) position in one of the rings determines the mechanisms of action of the flavonoids and reveals a complex multifunctional activity. Flavonoids have been widely used for their antioxidant, analgesic, and anti-inflammatory effects along with safe preclinical and clinical profiles. In this review, we discuss the preclinical and clinical evidence on the analgesic and anti-inflammatory proprieties of flavonoids. We also focus on how the development of formulations containing flavonoids, along with the understanding of their structure-activity relationship, can be harnessed to identify novel flavonoid-based therapies to treat pathological pain and inflammation.

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Protective role of apigenin on rotenone induced rat model of Parkinson's disease: Suppression of neuroinflammation and oxidative stress mediated apoptosis

Cited by 152 publications

References 112 publications

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

Therapeutic Potential of Flavonoids in Pain and Inflammation: Mechanisms of Action, Pre-Clinical and Clinical Data, and Pharmaceutical Development

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