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 10 publications

(2 citation statements)

References 53 publications

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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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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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“…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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Therapeutic Effect of Levetiracetam Against Thioacetamide-Induced Hepatic Encephalopathy Through Inhibition of Oxidative Stress and Downregulation of NF-κB, NLRP3, iNOS/NO, Pro-Inflammatory Cytokines and Apoptosis

Amirshahrokhi,

Imani

2024

Inflammation

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Hepatoprotective and neuroprotective effect of taxifolin on hepatic encephalopathy in rats

Cited by 10 publications

References 53 publications

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

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

Therapeutic Effect of Levetiracetam Against Thioacetamide-Induced Hepatic Encephalopathy Through Inhibition of Oxidative Stress and Downregulation of NF-κB, NLRP3, iNOS/NO, Pro-Inflammatory Cytokines and Apoptosis

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