Dietary cucurbitacin E reduces high-strength altitude training induced oxidative stress, inflammation and immunosuppression

Xie, Hui; Tuo, Xinling; Zhang, Feng; Bowen, Laura; Zhao, Wei; Xu, Yuyou

doi:10.1590/0001-3765202020200012

Cited by 11 publications

(12 citation statements)

References 31 publications

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“…Subsequently, electrical inactivity, edema, microangiopathy, and vascular resistance unite to cause irrevocable damage to the brain leading to extensive neurobehavioral discrepancies (Dong et al, 2018). Findings from prior studies suggest that cucurbitacins, particularly CuE, modulate diverse molecular targets and pathways that may protect against hypoperfusion states (Murtaza et al, 2017;Song et al, 2018;Xie et al, 2020). Although a few studies indicate promising effects of CuE in neurodegenerative disorders (Arel-Dubeau et al, 2014), nevertheless, the potential of CuE against perfusion defects has received very little emphasis so far.…”

Section: Discussionmentioning

confidence: 99%

“…In earlier studies, cucurbitacin showed cytotoxic, antitumor, hepatoprotective, anti-inflammatory, antimicrobial, anthelmintic, cardiovascular, and antidiabetic effects (Dhiman et al, 2012;Chung et al, 2015;Kaushik et al, 2015;Garg et al, 2018;Zhong et al, 2020). Many of the pharmacological activities (e.g., antiproliferative, antiobesity, immunomodulatory, and neuroprotective) of Cucurbitacin E (CuE) are attributed to antioxidant and anti-inflammatory properties (Murtaza et al, 2017;Song et al, 2018;Xie et al, 2020). CuE can modulate several molecular mechanisms (e.g., Janus kinase, signal transducer and activator of transcription, cyclo-oxygenase-2, autophagy, cofilin) that may be exploited for potential benefits in various cerebral disorders (Murtaza et al, 2017;Song et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

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The Mechanisms of Cucurbitacin E as a Neuroprotective and Memory-Enhancing Agent in a Cerebral Hypoperfusion Rat Model: Attenuation of Oxidative Stress, Inflammation, and Excitotoxicity

Kumar

Devi

et al. 2021

Front. Pharmacol.

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Impaired cerebral hemodynamic autoregulation, vasoconstriction, and cardiovascular and metabolic dysfunctions cause cerebral hypoperfusion (CH) that triggers pro-oxidative and inflammatory events. The sequences linked to ion-channelopathies and calcium and glutamatergic excitotoxicity mechanisms resulting in widespread brain damage and neurobehavioral deficits, including memory, neurological, and sensorimotor functions. The vasodilatory, anti-inflammatory, and antioxidant activities of cucurbitacin E (CuE) can alleviate CH-induced neurobehavioral impairments. In the present study, the neuroprotective effects of CuE were explored in a rat model of CH. Wistar rats were subjected to permanent bilateral common carotid artery occlusion to induce CH on day 1 and administered CuE (0.25, 0.5 mg/kg) and/or Bay-K8644 (calcium agonist, 0.5 mg/kg) for 28 days. CH caused impairment of neurological, sensorimotor, and memory functions that were ameliorated by CuE. CuE attenuated CH-triggered lipid peroxidation, 8-hydroxy-2′-deoxyguanosine, protein carbonyls, tumor necrosis factor-α, nuclear factor-kappaB, myeloperoxidase activity, inducible nitric oxide synthase, and matrix metalloproteinase-9 levels in brain resulting in a decrease in cell death biomarkers (lactate dehydrogenase and caspase-3). CuE decreased acetylcholinesterase activity, glutamate, and increased γ-aminobutyric acid levels in the brain. An increase in brain antioxidants was observed in CuE-treated rats subjected to CH. CuE has the potential to alleviate pathogenesis of CH and protect neurological, sensorimotor, and memory functions against CH.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Mechanisms of Cucurbitacin E as a Neuroprotective and Memory-Enhancing Agent in a Cerebral Hypoperfusion Rat Model: Attenuation of Oxidative Stress, Inflammation, and Excitotoxicity

Kumar

Devi

et al. 2021

Front. Pharmacol.

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“…We also showed that cucurbitacin B inhibited IL-1α-induced ICAM-1 expression in A549 cells. Previous studies reported that cucurbitacins suppressed the NF-κB pathway activated either constitutively or by various stimuli, including TNF-α, lipopolysaccharide, and phorbol ester plus ionomycin [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]. Different sets of receptors and adaptor proteins are involved in NF-κB signaling pathways, which converge to induce the activation of IκB kinase [3,9].…”

Section: Discussionmentioning

confidence: 99%

“…Cucurbitacins exert various biological effects, such as anti-inflammatory and anticancer activities [14][15][16][17][18]. The antiinflammatory and anticancer activities of cucurbitacins are attributed at least partly to their inhibition of the constitutive and stimulation-induced NF-κB-dependent pathway [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]. Cucurbitacin B was shown to down-regulate the TNF-α-induced expression of NF-κB target genes and inhibit the transactivation activity of RelA without suppressing its nuclear translocation in human cervical carcinoma HeLa cells [21].…”

Section: Introductionmentioning

confidence: 99%

Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

Kusagawa

Okuda

Yamaguchi

et al. 2022

IJMS

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Pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), induce the expression of intracellular adhesion molecule-1 (ICAM-1) by activating the nuclear factor κB (NF-κB) signaling pathway. In the present study, we found that cucurbitacin B decreased the expression of ICAM-1 in human lung adenocarcinoma A549 cells stimulated with TNF-α or interleukin-1α. We further investigated the mechanisms by which cucurbitacin B down-regulates TNF-α-induced ICAM-1 expression. Cucurbitacin B inhibited the nuclear translocation of the NF-κB subunit RelA and the phosphorylation of IκBα in A549 cells stimulated with TNF-α. Cucurbitacin B selectively down-regulated the expression of TNF receptor 1 (TNF-R1) without affecting three adaptor proteins (i.e., TRADD, RIPK1, and TRAF2). The TNF-α-converting enzyme inhibitor suppressed the down-regulation of TNF-R1 expression by cucurbitacin B. Glutathione, N-acetyl-L-cysteine, and, to a lesser extent, L-cysteine attenuated the inhibitory effects of cucurbitacin B on the TNF-α-induced expression of ICAM-1, suggesting that an α,β-unsaturated carbonyl moiety is essential for anti-inflammatory activity. The present results revealed that cucurbitacin B down-regulated the expression of TNF-R1 at the initial step in the TNF-α-dependent NF-κB signaling pathway.

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“…Cucurbitacin E ( 185 ), isolated from different plant species, can inhibit the expression of some cytokines, such as TNF‐α, and also downregulate the NF‐κB signaling pathway, which improves the pro‐inflammatory factors and proliferation activities of pro‐lymphocytes (Xie et al, 2020).…”

Section: Antiinflammatory Activity Of Natural Triterpenesmentioning

confidence: 99%

Antiinflammatory activity of natural triterpenes—An overview from 2006 to 2021

Miranda

Jesus

Luiz

et al. 2022

Phytotherapy Research

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Terpenes are one of the most abundant classes of secondary metabolites produced by plants and can be divided based on the number of isoprene units (C5) in monoterpenes (2 units—C10), sesquiterpenes (3 units—C15), diterpenes (4 units—C20), triterpenes (6 units—C30), etc. Chemically, triterpenes are classified based on their structural skeleton including lanostanes, euphanes, cycloartanes, ursanes, oleananes, lupanes, tirucallanes, cucurbitanes, dammaranes, baccharanes, friedelanes, hopanes, serratanes etc. Additionally, glycosylated (saponins) or highly oxidated/degraded (limonoids) triterpenes could be found in nature. The antiinflammatory effect and action as immunomodulators of these secondary metabolites have been demonstrated in different studies. This review reports an overview of articles published in the last 15 years (from 2006 to 2021 using PubMed and SciFinder database) describing the antiinflammatory effects of different triterpenes with their presumed mechanism of action, suggesting that triterpenes could be appointed as natural products with future pharmaceutical applicability.

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Dietary cucurbitacin E reduces high-strength altitude training induced oxidative stress, inflammation and immunosuppression

Cited by 11 publications

References 31 publications

The Mechanisms of Cucurbitacin E as a Neuroprotective and Memory-Enhancing Agent in a Cerebral Hypoperfusion Rat Model: Attenuation of Oxidative Stress, Inflammation, and Excitotoxicity

The Mechanisms of Cucurbitacin E as a Neuroprotective and Memory-Enhancing Agent in a Cerebral Hypoperfusion Rat Model: Attenuation of Oxidative Stress, Inflammation, and Excitotoxicity

Cucurbitacin B Down-Regulates TNF Receptor 1 Expression and Inhibits the TNF-α-Dependent Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

Antiinflammatory activity of natural triterpenes—An overview from 2006 to 2021

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