Corilagin inhibits the double strand break-triggered NF-κB pathway in irradiated microglial cells

Dong, Xiaorong; Luo, Mi; Fan, Li; Zhang, Tao; Liu, Li; Dong, Jing; Wu, Gang

doi:10.3892/ijmm_00000374

Cited by 22 publications

(2 citation statements)

References 20 publications

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“…We also found that QC reduced the levels of TNF-α and IL-1β in the serum and livers of mice. It has been demonstrated that corilagin and polydatin inhibit NF-κB activation 33–35 , and in agreement with this finding, QC inhibited the phosphorylation of p65 and thus inactivated the NF-κB pathway in mice with DEN-induced liver cancer. All these data indicate that NF-κB signaling is involved in the mechanism underlying the effects of QC in preventing or reducing the prevalence of hepatitis and hepatic cancers in mice.…”

Section: Discussionsupporting

confidence: 57%

Extracts of Qizhu decoction inhibit hepatitis and hepatocellular carcinoma in vitro and in C57BL/6 mice by suppressing NF-κB signaling

Wan

Shen

Wang

et al. 2019

Sci Rep

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Hepatitis and hepatocellular carcinoma are serious human diseases. Here, we examined the in vivo and in vitro inhibitory effect of extracts of Qizhu decoction (a traditional Chinese medicine) on hepatitis caused by diethylnitrosamine or hepatitis B virus and on diethylnitrosamine-induced hepatocellular carcinoma. The results showed that both the aqueous and ethanol extracts (QC and QS, respectively) of Qizhu decoction significantly inhibited hepatic inflammation and liver cancer induced by diethylnitrosamine or hepatitis B virus by suppressing NF-κB signaling and decreasing the levels of TNF-α and IL-1β. Both QC and QS inhibited the proliferation and migration of primary cancer hepatocytes by reducing cyclin B1, cyclin D1 and N-cadherin expression and increasing E-cadherin expression. QC and QS also promoted the apoptosis of primary cancer hepatocytes by upregulating caspase-3 and downregulating BCL-2 expression. The knockdown of p65 in NF-κB signaling inhibited the ability of QC and QS to significantly reduce the colony formation ability of liver cancer cells. Additionally, QC and QS might significantly inhibit the DNA replication of hepatitis B virus in vivo and in vitro, and we found that corilagin and polydatin were the active compounds of QC and QS. Taken together, our in vitro findings and our results in C57BL/6 mice showed that extracts of Qizhu decoction might inhibit hepatitis and hepatocellular carcinoma by suppressing NF-κB signaling.

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Section: Discussionsupporting

confidence: 57%

Extracts of Qizhu decoction inhibit hepatitis and hepatocellular carcinoma in vitro and in C57BL/6 mice by suppressing NF-κB signaling

Wan

Shen

Wang

et al. 2019

Sci Rep

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“…A possible mechanism on how microglia are activated is by IR-induced double-strand breaks, which trigger the NFκB pathway-mediated production of inflammatory proteins (73). Microglial cells in their activated state secrete a panel of pro-inflammatory cytokines, which inhibit neurogenesis in the hippocampus by disrupting neurogenic signaling pathways.…”

Section: Inflammation-mediated Mechanisms In Radiation-induced Brain mentioning

confidence: 99%

Ionizing Radiation-Induced Immune and Inflammatory Reactions in the Brain

2017

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Radiation-induced late brain injury consisting of vascular abnormalities, demyelination, white matter necrosis, and cognitive impairment has been described in patients subjected to cranial radiotherapy for brain tumors. Accumulating evidence suggests that various degrees of cognitive deficit can develop after much lower doses of ionizing radiation, as well. The pathophysiological mechanisms underlying these alterations are not elucidated so far. A permanent deficit in neurogenesis, chronic microvascular alterations, and blood–brain barrier dysfunctionality are considered among the main causative factors. Chronic neuroinflammation and altered immune reactions in the brain, which are inherent complications of brain irradiation, have also been directly implicated in the development of cognitive decline after radiation. This review aims to give a comprehensive overview on radiation-induced immune alterations and inflammatory reactions in the brain and summarizes how these processes can influence cognitive performance. The available data on the risk of low-dose radiation exposure in the development of cognitive impairment and the underlying mechanisms are also discussed.

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Aging‐like changes in the transcriptome of irradiated microglia

Burns

Kumar

et al. 2015

Glia

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Whole brain irradiation remains important in the management of brain tumors. Although necessary for improving survival outcomes, cranial irradiation also results in cognitive decline in long-term survivors. A chronic inflammatory state characterized by microglial activation has been implicated in radiation-induced brain injury. We here provide the first comprehensive transcriptional profile of irradiated microglia. Fluorescence-activated cell sorting (FACS) was used to isolate CD11b+ microglia from the hippocampi of C57BL/6 and Balb/c mice 1 month after 10Gy cranial irradiation. Affymetrix gene expression profiles were evaluated using linear modeling, rank product analyses. One month after irradiation, a conserved irradiation signature across strains was identified, comprising 448 and 85 differentially up- and down-regulated genes, respectively. Gene set enrichment analysis (GSEA) demonstrated enrichment for inflammation, including M1 macrophage-associated genes, but also an unexpected enrichment for extracellular matrix and blood coagulation-related gene sets, in contrast previously described microglial states. Weighted gene co-expression network analysis (WGCNA) confirmed these findings and further revealed alterations in mitochondrial function. The RNA-seq transcriptome of microglia 24h post-radiation proved similar to the 1-month transcriptome, but additionally featured alterations in apoptotic and lysosomal gene expression. Re-analysis of published aging mouse microglia transcriptome data demonstrated striking similarity to the 1 month irradiated microglia transcriptome, suggesting that shared mechanisms may underlie aging and chronic irradiation-induced cognitive decline.

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Corilagin inhibits the double strand break-triggered NF-κB pathway in irradiated microglial cells

Cited by 22 publications

References 20 publications

Extracts of Qizhu decoction inhibit hepatitis and hepatocellular carcinoma in vitro and in C57BL/6 mice by suppressing NF-κB signaling

Extracts of Qizhu decoction inhibit hepatitis and hepatocellular carcinoma in vitro and in C57BL/6 mice by suppressing NF-κB signaling

Ionizing Radiation-Induced Immune and Inflammatory Reactions in the Brain

Aging‐like changes in the transcriptome of irradiated microglia

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