“…It also relates to betanin's effect on mRNA and on the protein expression of antioxidative enzymes (Krajka-Kuzniak et al 2013). The protection against oxidative stress-induced apoptotic death in PC 12 cells 6-OHDA exposed an association with SAPK/JNK, and partial PI3 K inhibition was also recently reported (Hadipour et al 2020). We indicated betanin's protective effect against neurodegeneration in nigrostriatal structures such as SNc and Str, along with dopaminergic neuron preservation in these two areas.…”
The present study aimed to investigate betanin’s neuroprotective effect in mice with rotenone-induced Parkinson-like motor dysfunction and neurodegeneration. Forty male ICR mice were divided into 4 groups: Sham-veh, Rot-veh, Rot-Bet100 and Rot-Bet200. Rotenone (Rot) at 2.5 mg/kg/48 h was subcutaneous injected, and betanin (Bet) at 100 and 200 mg/kg/48 h were given alternately with the Rot injections in Rot-Bet groups for 6 weeks. Motor dysfunctions were evaluated weekly using hanging wire and rotarod tests. Malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), neuronal degeneration in the motor cortex (MC), striatum (Str) and substantia nigra par compacta (SNc) were evaluated. The immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in SNc were also measured. We found that rotenone significantly decreased the time to fall in a hanging wire test after the 4th week and after the rotarod test at the 6th week (p<0.05). The percentage of neuronal degeneration in MC, Str and SNc (p<0.05) significantly increased, and the TH density in Str and in SNc (p<0.05) significantly decreased. Betanin at 100 and 200 mg/kg significantly prevented MC, Str and SNc neuronal degeneration (p<0.05) and prevented the decrease of TH density in Str and in SNc (p<0.05). These findings appeared concurrently with improved effects on the time to fall in hanging wire and rotarod tests (p<0.05). Treatment with betanin significantly prevented increased MDA levels and boosted GSH, CAT and SOD activities (p<0.05). Betanin exhibits neuroprotective effects against rotenone-induced Parkinson in mice regarding both motor dysfunction and neurodegeneration. Betanin’s neurohealth benefit relates to its powerful antioxidative property. Therefore, betanin use in neurodegenerative disease therapy is interesting to study.
“…It also relates to betanin's effect on mRNA and on the protein expression of antioxidative enzymes (Krajka-Kuzniak et al 2013). The protection against oxidative stress-induced apoptotic death in PC 12 cells 6-OHDA exposed an association with SAPK/JNK, and partial PI3 K inhibition was also recently reported (Hadipour et al 2020). We indicated betanin's protective effect against neurodegeneration in nigrostriatal structures such as SNc and Str, along with dopaminergic neuron preservation in these two areas.…”
The present study aimed to investigate betanin’s neuroprotective effect in mice with rotenone-induced Parkinson-like motor dysfunction and neurodegeneration. Forty male ICR mice were divided into 4 groups: Sham-veh, Rot-veh, Rot-Bet100 and Rot-Bet200. Rotenone (Rot) at 2.5 mg/kg/48 h was subcutaneous injected, and betanin (Bet) at 100 and 200 mg/kg/48 h were given alternately with the Rot injections in Rot-Bet groups for 6 weeks. Motor dysfunctions were evaluated weekly using hanging wire and rotarod tests. Malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), neuronal degeneration in the motor cortex (MC), striatum (Str) and substantia nigra par compacta (SNc) were evaluated. The immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in SNc were also measured. We found that rotenone significantly decreased the time to fall in a hanging wire test after the 4th week and after the rotarod test at the 6th week (p<0.05). The percentage of neuronal degeneration in MC, Str and SNc (p<0.05) significantly increased, and the TH density in Str and in SNc (p<0.05) significantly decreased. Betanin at 100 and 200 mg/kg significantly prevented MC, Str and SNc neuronal degeneration (p<0.05) and prevented the decrease of TH density in Str and in SNc (p<0.05). These findings appeared concurrently with improved effects on the time to fall in hanging wire and rotarod tests (p<0.05). Treatment with betanin significantly prevented increased MDA levels and boosted GSH, CAT and SOD activities (p<0.05). Betanin exhibits neuroprotective effects against rotenone-induced Parkinson in mice regarding both motor dysfunction and neurodegeneration. Betanin’s neurohealth benefit relates to its powerful antioxidative property. Therefore, betanin use in neurodegenerative disease therapy is interesting to study.
“…Additionally, betanin has been shown to exhibit hepatoprotective properties against acetaminophen-induced hepatic injury in a rat model, which was confirmed by histopathological data [48]. Moreover, betanin has also been demonstrated to possess antiapoptotic properties [46]. Last but not least, betalain-rich concentrates have been shown to improve running, cycling and exercise performances [49,50].…”
Section: Introductionmentioning
confidence: 82%
“…In an attempt to unravel the mechanistic pathway beyond these potential protective effects, the authors have examined the protein levels of survivin and cytochrome c. It appeared that pretreatment with betanin has resulted in an increased protein level of survivin with a concomitant reduction in cytochrome c when compared to the 6-OHDA treated cells. Moreover, 6-OHDA resulted in an increased Phospho SAPK/JNK46/54 to SAPK/ JNK46/54 proteins relative to the control group, a finding that was reverted as a consequence of betanin pretreatment [46]. However, it should be noted that these beneficial protective effects of betanin against a Parkinson's like model are only demonstrated in vitro.…”
Section: Betanin and Oxidative Stressmentioning
confidence: 92%
“…The authors have depicted that pretreatment with different concentrations of betanin ranging from 5-200 μM was able to significantly lower the level of the fluorescent signal indicating a lower level of reactive oxygen species. The results were further augmented by having significantly better cell viability and survival with betanin pretreatment, especially in light of the fact that exposing the cultured cells to such concentrations of betanin was ultimately safe as assessed by cytotoxicity studies [46]. Relevant results were illustrated in primary rat hepatocytes exposed to organophosphate poisoning and in Huh7 human liver hepatoma cells [60,61].…”
Section: Betanin and Oxidative Stressmentioning
confidence: 99%
“…Betanin is formed by β-glycosylation of the aglycone betanidin C5 [39] as shown in Figure 2, with a molecular weight of 550 g/mol [40]. A marked number of studies have asserted the potential beneficial therapeutic effects of betanin in a number of conditions and diseases, among which are renal fibrosis, atherosclerotic diseases, and cancers [32, 41,42], in addition to its well documented antioxidative properties in Parkinson's disease, peripheral artery vasospasm models and others [43][44][45][46].…”
Plants with medicinal properties possess beneficial influences on health and disease. Different plant parts and extracts carry valuable active ingredients with pharmacological properties that lead to developing new drugs. Terminalia bellirica is among those plants that have been formulated as pharmaceutical products. This is attributed to its biologically active phenolics and tannins exhibiting analgesic, anti-hypertensive, anti-microbial, anti-diabetic, anti-oxidant, as well as, other pharmacological properties. Beetroot has been shown to be rich in nitrates with a positive impact on the cardiovascular system. Beetroot contains a number of useful ingredients as the free-radical scavenger ascorbic acid, the anti-inflammatory flavonoids and the anti-oxidant carotenoids. Moreover, beetroot is rich in the natural colorant betalains that are further classified into betacyanins and betaxanthins. Betanin, is one of the major constituents of beetroots that have been postulated to possess significant beneficial therapeutic effects in a number of conditions and diseases. However, several studies have demonstrated the relatively poor bioavailability of betanin upon oral administration. In the current review we aim to highlight some of the latest researches dealing with the therapeutic properties of betanin in different disease conditions, the possible mechanistic pathways beyond such beneficial effects and plausible strategies capable of enhancing its stability and bioavailability.
Due to many therapeutic effects, Ginger (Zingiber officinale) is the most widely used spice around the world, including in Iran. Due to its potent anti-inflammatory and antioxidant effects, ginger may protect against neurodegenerative disorders. Here, we investigated the effects of 6-gingerol (the main bioactive compound in ginger) on 6-hydroxydopamine (6-OHDA)-induced cell death in PC12 cells. Cell viability, cell apoptosis, and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and survivin expression were measured using resazurin, propidium iodide (PI) and flow cytometry, and western blot analysis. 6-OHDA (100 μM) reduced the cell viability, increased apoptosis, increased the active form of SAPK/JNK, and decreased survivin protein level in PC12 exposed cells in a dose and time-dependent manner.Pretreatment with 6-gingerol significantly increased the viability and reduced apoptosis (2.5 and 5 µM). Also, pretreatment with 6-gingerol at 2.5 and 5 µM increased survivin whereas, 6-gingerol at 2.5 µM reduced (P-SAPK/JNK):(SAPK/JNK) levels to a level near that of the related control. According to the results, 6-gingerol blocks 6-OHDA-induced cell damage by suppressing oxidative stress and antiapoptotic activity. Thus, 6-gingerol may process beneficial protective effects in slowing the progression of Parkinson's disease.
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