Hepatoprotective and neuroprotective effect of taxifolin on hepatic encephalopathy in rats

Okkay, Ufuk; Okkay, Irmak Ferah; Çiçek, Betül; Aydin, İsmail Hakkı; Özkaraca, Mustafa

doi:10.1007/s11011-022-00952-3

Cited by 19 publications

(14 citation statements)

References 53 publications

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“…There are no studies showing the effect of taxifolin on As-induced neurotoxicity. However, a previous study revealed that taxifolin treatment of rats with hepatic encephalopathy makes inhibition of ROS generation and MDA levels as well as an elevation in the content of GSH replenishment and improved antioxidant defense in hippocampus cells, which was in support of our work [17]. Taxifolin through inhibition of production of free radicals and restoration of oxidized membrane phospholipids displayed profitable effects against oxidative injury [25].…”

Section: Taxifolin Alleviates Oxidative Stress Promoted By Naaso2supporting

confidence: 86%

“…As evidenced in the current report, the level of IL-17A besides activated other cytokines was associated with the As-related inflammatory response in the hippocampus. As was demonstrated to augment the levels of inflammatory cytokines inclusive of TNF-α, IL-1β and IL-6 in rats's hippocampus [17]. Pre-treatment with taxifolin at all concentrations for 1h followed by exposure to 10 µM NaAsO2 for 24 h significantly declined the levels of TNF-α, IL-1β, and IL-6 in comparison to those of only NaAsO2 exposure HT-22 cells (P < .05).…”

Section: Taxifolin Alleviates Oxidative Stress Promoted By Naaso2mentioning

confidence: 85%

“…Taxifolin is a flavonoid compound, that originally existed in many plants like French maritime pine bark and milk thistle and is also used in commercial preparations [16]. Taxifolin has a variety of pharmacological actions, the most essential among which are antioxidant and anti-inflammatory features [17]. Iwasa et al revealed that taxifolin suppresses IL-1β generation by reducing the intracellular ROS levels in inflammatory responses to high-glucose-stimulated mouse microglial cells [18].…”

Section: Introductionmentioning

confidence: 99%

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Taxifolin ameliorates IL-17A-enhanced hippocampal inflammation and oxidative stress in arsenic-exposed HT-22 cells

Betul Cicek,

Betul Danısman

2023

World J. Adv. Res. Rev.

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Arsenic (As) promotes neuronal damage in the hippocampus which is associated with cognitive function. Taxifolin, a flavonol with strong anti-oxidative and anti-inflammatory properties, is known to have beneficial properties in neurodegeneration, but its effect on As-induced hippocampal damage is unknown. Here, we explored whether taxifolin has therapeutic potential in ameliorating as causing toxicity in mouse hippocampal HT-22 cells, hypothesizing that inhibiting oxido-inflammation stress may reverse As-associated damage through several pathways. Findings indicate that pretreatment with taxifolin reversed the reduction of sodium arsenite (NaAsO2) induced cell death. In addition, taxifolin ameliorated NaAsO2-related oxidative stress as measured by the formation of ROS, MDA level and GSH content. Moreover, we revealed the taxifolin treatment resulted in a reduction of IL-17A level and subsequent diminished activation of TNF-α, IL-1β, and IL-6 concentrations in HT-22 cells treated with NaAsO2. These findings imply when considered collectively, HT-22 cells are shielded by taxifolin from NaAsO2-evoked oxidative cell death and neuroinflammation. Thus, our report indicates that has a protective role in hippocampal cell culture systems.

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Section: Taxifolin Alleviates Oxidative Stress Promoted By Naaso2supporting

confidence: 86%

Section: Taxifolin Alleviates Oxidative Stress Promoted By Naaso2mentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

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Taxifolin ameliorates IL-17A-enhanced hippocampal inflammation and oxidative stress in arsenic-exposed HT-22 cells

Betul Cicek,

Betul Danısman

2023

World J. Adv. Res. Rev.

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“…From the perspective of regulating oxidative stress and apoptosis of GIONFH, we explored therapeutic drugs with potential antioxidative stress and antiapoptotic effects. TAX, as a natural antioxidant, has shown antioxidative stress and antiapoptosis effects in other models (Okkay et al, 2022; Sun et al, 2014). However, the role of TAX in GIONFH remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Taxifolin‐mediated Nrf2 activation ameliorates oxidative stress and apoptosis for the treatment of glucocorticoid‐induced osteonecrosis of the femoral head

Jiang,

Lin,

Cai

et al. 2023

Phytotherapy Research

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Glucocorticoid‐induced osteonecrosis of the femoral head (GIONFH) is the main complication secondary to long‐term or excessive use of glucocorticoids (GCs). Taxifolin (TAX) is a natural antioxidant with various pharmacological effects, such as antioxidative stress and antiapoptotic properties. The purpose of this study was to explore whether TAX could regulate oxidative stress and apoptosis in GIONFH by activating the nuclear factor erythroid 2‐related factor 2 (Nrf2) pathway. We conducted qRT‐PCR, Western blotting, TUNEL assays, flow cytometry, and other experiments in vitro. Microcomputed tomography analysis, hematoxylin–eosin staining, and immunohistochemical staining were performed to determine the therapeutic effect of TAX in vivo. TAX mitigated the overexpression of ROS and NOX gene expression induced by DEX, effectively reducing oxidative stress. Additionally, TAX could alleviate DEX‐induced osteoblast apoptosis, as evidenced by qRT‐PCR, Western blotting, and other experimental techniques. Our in vivo studies further demonstrated that TAX mitigates the progression of GIONFH in rats by combating oxidative stress and apoptosis. Mechanistic exploration revealed that TAX thwarts the progression of GIONFH through the activation of the Nrf2 pathway. Overall, our research herein reports that TAX‐mediated Nrf2 activation ameliorates oxidative stress and apoptosis for the treatment of GIONFH.

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“…In addition, the apoptosis mechanism was improved by maintaining the mRNA expression level of BCl-2, an anti-apoptotic factor, at an almost normal level [ 49 ]. Taxifolin, a major bioactive component of KRPBE, ultimately reversed neurobehavioral disorders through hepatic and neuroprotective roles by regulating antioxidant capacity, pro-inflammatory mediators and levels of BAX and BCl-2 against thioacetamide-induced hepatic encephalopathy [ 75 ]. In addition, PCA showed neuroprotective properties by inhibiting the activation of neuro-oxidative damage and inflammatory response induced by arsenic exposure, downregulating BAX and caspase 3, and upregulating BCl-2 and BDNF [ 76 ].…”

Section: Discussionmentioning

confidence: 99%

Korean Red Pine (Pinus densiflora) Bark Extract Attenuates Aβ-Induced Cognitive Impairment by Regulating Cholinergic Dysfunction and Neuroinflammation

Kim

Kang

et al. 2022

J. Microbiol. Biotechnol.

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In this study, we investigated the anti-amnesic effect of Korean red pine (Pinus densiflora) bark extract (KRPBE) against amyloid beta 1-42 (Aβ 1-42 )-induced neurotoxicity. We found that treatment with KRPBE improved the behavioral function in Aβ-induced mice, and also boosted the antioxidant system in mice by decreasing malondialdehyde (MDA) content, increasing superoxide dismutase (SOD) activities, and reducing glutathione (GSH) levels. In addition, KRPBE improved the cholinergic system by suppressing reduced acetylcholine (ACh) content while also activating acetylcholinesterase (AChE), regulating the expression of choline acetyltransferase (ChAT), postsynaptic density protein-95 (PSD-95), and synaptophysin. KRPBE also showed an ameliorating effect on cerebral mitochondrial deficit by regulating reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP levels. Moreover, KRPBE modulated the expression levels of neurotoxicity indicators Aβ and phosphorylated tau (p-tau) and inflammatory cytokines TNF-α, p-IκB-α, and IL-1β. Furthermore, we found that KRPBE improved the expression levels of neuronal apoptosis-related markers BAX and BCl-2 and increased the expression levels of BDNF and p-CREB. Therefore, this study suggests that KRPBE treatment has an anti-amnestic effect by modulating cholinergic system dysfunction and neuroinflammation in Aβ 1-42 -induced cognitive impairment in mice.

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Hepatoprotective and neuroprotective effect of taxifolin on hepatic encephalopathy in rats

Cited by 19 publications

References 53 publications

Taxifolin ameliorates IL-17A-enhanced hippocampal inflammation and oxidative stress in arsenic-exposed HT-22 cells

Taxifolin ameliorates IL-17A-enhanced hippocampal inflammation and oxidative stress in arsenic-exposed HT-22 cells

Taxifolin‐mediated Nrf2 activation ameliorates oxidative stress and apoptosis for the treatment of glucocorticoid‐induced osteonecrosis of the femoral head

Korean Red Pine (Pinus densiflora) Bark Extract Attenuates Aβ-Induced Cognitive Impairment by Regulating Cholinergic Dysfunction and Neuroinflammation

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