Didymin ameliorates hepatic injury through inhibition of MAPK and NF-κB pathways by up-regulating RKIP expression

Huang, Quanfang; Bai, Facheng; Nie, Jinlan; Lu, Sheng; Lu, Chunyuang; Zhu, Xunshuai; Zhuo, Lang; Lin, Xiaobo

doi:10.1016/j.intimp.2016.11.028

Cited by 32 publications

(25 citation statements)

References 28 publications

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“…Additionally, it was described that the flavone didymin, isolated from Origanum vulgare, significantly ameliorated liver injury in mice by in part reducing the levels of pro-inflammatory cytokines, such as TNF-α, IL-6 and IL-1β ( Figure 1). Didymin also enhanced RKIP expression, resulting in inhibition of the MAPK and NF-κB signalling pathways, which also contributed to its anti-inflammatory effect [53]. Furthermore, a study showed a decreased RKIP expression and increased NF-κB activation in renal tissues of rats with diabetic nephropathy (Figure 1), again supporting an inhibitory role for RKIP in NF-κB mediated inflammatory responses.…”

Section: Rkip and Inflammationmentioning

confidence: 79%

RKIP as an Inflammatory and Immune System Modulator: Implications in Cancer

et al. 2019

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Raf kinase inhibitor protein (RKIP), an important modulator of intracellular signalling pathways, is commonly downregulated in multiple cancers. This reduction, or loss of expression, is correlated not only with the presence of metastasis, contributing to RKIP’s classification as a metastasis suppressor, but also with tumour aggressiveness and poor prognosis. Recent findings suggest a strong involvement of RKIP in the modulation of tumour microenvironment components, particularly by controlling the infiltration of specific immune cells and secretion of pro-metastatic factors. Additionally, RKIP interaction with multiple signalling molecules seems to potentiate its function as a regulator of inflammatory processes, mainly through stimulation of anti- or pro-inflammatory cytokines. Furthermore, RKIP is involved in the modulation of immunotherapeutic drugs response, through diverse mechanisms that sensitize cells to apoptosis. In the present review, we will provide updated information about the role of RKIP as an inflammatory and immune modulator and its potential implications in cancer will be addressed.

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Section: Rkip and Inflammationmentioning

confidence: 79%

RKIP as an Inflammatory and Immune System Modulator: Implications in Cancer

et al. 2019

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“…A growing number of studies reported that NF‐κB is a critical transcriptional factor and played a major role in the inflammatory response in kidneys of patients with progressive DN (Garcia‐Garcia, Getino‐Melián, Domínguez‐Pimentel, & Navarro‐Gonzále, ). Studies showed that IL‐8, FN, and PAI‐1 expression were partially NF‐κB dependent (Huang et al, ). To assess the inhibitory effects of celastrol on the inflammatory response, we examined the effects of celastrol on NF‐κB activity in renal tissues by western blotting.…”

Section: Discussionmentioning

confidence: 99%

Celastrol attenuates renal injury in diabetic rats via MAPK/NF‐κB pathway

Zhang

Cao

Yang

et al. 2019

Phytotherapy Research

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The purpose of this study was to investigate the renal protective effect of celastrol on diabetic rats. Furthermore, the mechanism of its action was discussed whether it was related to MAPK/NF-κB signaling pathway. There were a total of 36 rats. Six rats were randomly chosen as the control group. The remaining 30 rats were given 1% streptozotocin intraperitoneal injection (50 mg/kg) and were randomly divided into five groups: the model control group, the low-dose celastrol group, the high-dose celastrol group, the Tripterygium wilfordii polyglycosides group, and the MAPK/NF-κB inhibitor group. After 4 weeks of continuous administration, 24-hr urine volume, urinary protein, blood urea nitrogen, and serum creatinine content were observed, and hematoxylin-eosin (HE) staining of the kidney and liver were evaluated.

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“…However, excessive hepatocyte apoptosis is likely to contribute to ALI by causing liver dysfunction [ 7 ]. Natural killer cells, T cells, and macrophages are mobilized during ALI, and liver-resident macrophages act as a factor contributing to liver damage by mass production of cytokines in response to inflammatory stimuli [ 8 ]. These inflammatory cells secrete pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, and these pro-inflammatory cytokines play a role in promoting ALI progression.…”

Section: Introductionmentioning

confidence: 99%

Polydeoxyribonucleotide Exerts Protective Effect Against CCl4-Induced Acute Liver Injury Through Inactivation of NF-κB/MAPK Signaling Pathway in Mice

Jin

Hwang

et al. 2020

IJMS

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Acute liver injury (ALI) causes life-threatening clinical problem, and its underlying etiology includes inflammation and apoptosis. An adenosine A2A receptor agonist, polydeoxyribonucleotide (PDRN), exhibits anti-inflammatory and anti-apoptotic effects by inhibiting the secretion of pro-inflammatory cytokines. In the current study, the protective effect of PDRN against carbon tetrachloride (CCl4)-induced ALI was investigated using mice. For the induction of ALI, mice received intraperitoneal injection of CCl4 twice over seven days. Mice from the PDRN-treated groups received an intraperitoneal injection of 200 μL saline containing PDRN (8 mg/kg), once a day for seven days, starting on day 1 after the first CCl4 injection. In order to confirm that the action of PDRN occurs through the adenosine A2A receptor, 8 mg/kg 3,7-dimethyl-1-propargylxanthine (DMPX), an adenosine A2A receptor antagonist, was treated with PDRN. Administration of CCl4 impaired liver tissue and increased the liver index and histopathologic score. The expression of pro-inflammatory cytokines was increased, and apoptosis was induced by the administration of CCl4. Administration of CCl4 activated nuclear factor-kappa B (NF-κB) and facilitated phosphorylation of signaling factors in mitogen-activated protein kinase (MAPK). In contrast, PDRN treatment suppressed the secretion of pro-inflammatory cytokines and inhibited apoptosis. PDRN treatment inactivated NF-κB and suppressed phosphorylation of signaling factors in MAPK. As a result, liver index and histopathologic score were reduced by PDRN treatment. When PDRN was treated with DMPX, the anti-inflammatory and anti-apoptotic effect of PDRN disappeared. Therefore, PDRN can be used as an effective therapeutic agent for acute liver damage.

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Didymin ameliorates hepatic injury through inhibition of MAPK and NF-κB pathways by up-regulating RKIP expression

Cited by 32 publications

References 28 publications

RKIP as an Inflammatory and Immune System Modulator: Implications in Cancer

RKIP as an Inflammatory and Immune System Modulator: Implications in Cancer

Celastrol attenuates renal injury in diabetic rats via MAPK/NF‐κB pathway

Polydeoxyribonucleotide Exerts Protective Effect Against CCl4-Induced Acute Liver Injury Through Inactivation of NF-κB/MAPK Signaling Pathway in Mice

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