Propofol attenuates intermittent hypoxia induced up-regulation of proinflammatory cytokines in microglia through inhibiting the activation of NF-Bκ/p38 MAPK signalling

Liu, Song; Sun, Jin; Lian, Ren; Chen, Kui; Xu, Bo

doi:10.5114/fn.2017.68579

Cited by 36 publications

(32 citation statements)

References 34 publications

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“…Liu et al. suggested that propofol attenuated intermittent hypoxia induced upregulation of proinflammatory cytokines in microglia through inhibiting the activation of NF‐κB/p38 MAPK signaling. Zhu et al.…”

Section: Discussionmentioning

confidence: 99%

Propofol inhibits pancreatic cancer progress under hypoxia via ADAM8

Gao

Zhang

et al. 2019

J Hepato Biliary Pancreat

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Background To investigate the potential anti-tumoral properties of propofol in pancreatic cancer and elucidate the underlying mechanisms. Methods The relative expression of ADAM metallopeptidase domain 8 (ADAM8) in response to hypoxia in Panc1 cells was analyzed by western blotting. The enzymatic activity was determined by fluorescence release from PEPDAB013 decomposition. Cell growth was measured via cell counting and cell viability was measured using CCK-8 kit. Cell migrative capacity was evaluated by transwell and adhesion assay. The relative abundance of angiogenesis-related markers including platelet-derived growth factor AA, angiogenin, endothelin-1 and vascular endothelial growth factor were determined by real-time polymerase chain reaction and western blotting. The antitumoral activity of propofol was investigated with Panc1derived xenograft mice model. Results ADAM8 was significantly induced by hypoxia and efficiently inhibited by co-treatment with propofol. Propofol suppressed proliferation and compromised viability of Panc1 cells. In addition, the migrative capacity was greatly inhibited by propofol dosage. Comprehensive profiling of angiogenesis-related markers demonstrated that propofol remarkably suppressed neovascularization response in Panc1 cells under hypoxia. We further uncovered that propofol administration via subcutaneous injection delayed xenograft tumor progression. Conclusion Propofol specifically inhibited ADAM8 expression and activation in response to hypoxia in pancreatic cancer, and held great value for therapeutic effects.

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Section: Discussionmentioning

confidence: 99%

Propofol inhibits pancreatic cancer progress under hypoxia via ADAM8

Gao

Zhang

et al. 2019

J Hepato Biliary Pancreat

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“…MAPK and NF-κB signaling pathways are confirmed to play crucial roles in inflammatory response (Chen et al 2018, Gao et al 2018. Suppressing the abnormal activation of MAPK and NF-κB pathways has been reported to attenuate IH-induced inflammation (Kang et al 2017, Liu et al 2017. Moreover, MAPK activation has also participated in IH-induced apoptosis (Wu et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Tempol Alleviates Chronic Intermittent Hypoxia-Induced Pancreatic Injury Through Repressing Inflammation and Apoptosis

Wang

Han

et al. 2019

Physiol Res

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Obstructive sleep apnea (OSA) has been demonstrated to be implicated in disorder of insulin secretion and diabetes mellitus. In this study, we aimed to evaluate the protective role of tempol, a powerful antioxidant, in chronic intermittent hypoxia (IH)-induced pancreatic injury. The rat model of OSA was established by IH exposure. The pathological changes, increased blood-glucose level, and raised proinsulin/insulin ratio in pancreatic tissues of rats received IH were effectively relieved by tempol delivery. In addition, the enhanced levels of pro-inflammatory cytokines, TNF-α, IL-1β, IL-6, and inflammatory mediators, PGE2, cyclooxygenase-2 (COX-2), NO, and inducible nitric oxide synthase (iNOS) in pancreatic tissue were suppressed by tempol. Moreover, tempol inhibited IH-induced apoptosis in pancreatic tissue as evidenced by upregulated Bcl-2 level, and downregulated Bax and cleaved caspase-3 levels. Finally, the abnormal activation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways induced by IH was restrained by tempol administration. In summary, our study demonstrates that tempol relieves IH-induced pancreatic injury by inhibiting inflammatory response and apoptosis, which provides theoretical basis for tempol as an effective treatment for OSA-induced pancreatic injury.

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“…Numerous experimental evidence suggests that many chronic inflammations can cause tumours, and the interaction between immune cells can stimulate tumour cell proliferation and angiogenesis (Amara & Tiriveedhi, ). Macrophages, neutrophils and other inflammatory cells often produce reactive oxygen species, resulting in protein and tissue damage and permanent DNA damage, and inflammatory processes also affect tumour progression (Liu, Sun, Ren, Chen, & Xu, ). There were three kinds of NOS isomers in the human cells, and the neuronal NOS (nNOS) and endothelial NOS (eNOS) constitutively expressed in the cells and produced NO at the nanomole level in the Ca 2+ ‐dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Differential research of inflammatory and related mediators in BPH, histological prostatitis and PCa

et al. 2018

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Prostate cancer (PCa) is one of the most common male malignancies in the world. It was aimed to investigate differential expression of inflammatory and related factors in benign prostatic hyperplasia (BPH), prostate cancer (PCa), histological prostatitis (HP) and explore the role of Inducible nitric oxide synthase (iNOS), (VEGF) Vascular endothelial growth factor, androgen receptor (AR) and IL-2, IL-8 and TNF-α in the occurrence and development of prostate cancer. RT-PCR was used to detect the mRNA expression level of iNOS, VEGF, AR and IL-2, IL-8 and TNF-α in BPH, PCa and BPH+HP. Western blotting and immunohistochemical staining were used to detect the protein levels of various proteins in three diseases. The results showed the mRNA and protein levels of iNOS, VEGF and IL-2, IL-8 and TNF-α were significantly increased in PCa and BPH+HP groups compared with BPH group (p < .05), while the AR was significantly lower than those in PCa and BPH+HP groups (p < .05). There was no significant difference in the mRNA and protein levels of iNOS, VEGF, AR and IL-2, IL-8 and TNF-α between PCa and BPH+HP groups (p > .05). iNOS, VEGF, AR and IL-2, IL-8 and TNF-α are involved in the malignant transformation of prostate tissue and play an important role in the development and progression of Prostate cancer (PCa).

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Propofol attenuates intermittent hypoxia induced up-regulation of proinflammatory cytokines in microglia through inhibiting the activation of NF-Bκ/p38 MAPK signalling

Cited by 36 publications

References 34 publications

Propofol inhibits pancreatic cancer progress under hypoxia via ADAM8

Propofol inhibits pancreatic cancer progress under hypoxia via ADAM8

Tempol Alleviates Chronic Intermittent Hypoxia-Induced Pancreatic Injury Through Repressing Inflammation and Apoptosis

Differential research of inflammatory and related mediators in BPH, histological prostatitis and PCa

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