NF‐kB signaling in cardiomyocytes is inhibited by sevoflurane and promoted by propofol

Oda-Kawashima, Keiko; Sedukhina, Anna S.; Okamoto, Naoki; Lytvyn, Mariya; Minagawa, Kimino; Iwata, Teppei; Kumai, Toshio; Sato, Eri; Inada, Eiichi; Yamaura, Ayako; Sakamoto, Miki; Roche-Molina, Marta; Bernal, Juan A.; Sato, Ko

doi:10.1002/2211-5463.12783

Cited by 4 publications

(3 citation statements)

References 31 publications

(44 reference statements)

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“…Several studies have reported that an HF diet is closely associated with inflammation [ 26 , 27 ]. NF-κB, one of the members in the family of transcription factors, often functions in most cells [ 28 ] and involves in the immune and inflammatory responses and affecting cell differentiation, apoptosis, and tissue damage [ 29 ]. It has been shown that an HF diet may induce high levels of IL-1β, IL-6, and TNFα by up-regulating the expression of TLR4 and NF-κB pathways [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Geniposide suppressed OX-LDL-induced osteoblast apoptosis by regulating the NRF2/NF-κB signaling pathway

Xiao,

Zhang,

et al. 2023

J Orthop Surg Res

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Background Osteoporosis (OP), due to microarchitectural alterations, is associated with decreased bone mass, declined strength, and increased fracture risk. Increased osteoblast apoptosis contributes to the progression of OP. Natural compounds from herbs provide a rich resource for drug screening. Our previous investigation showed that geniposide (GEN), an effective compound from Eucommia ulmoides, could protect against the pathological development of OP induced by cholesterol accumulation. Methods The rat OP models were duplicated. Dual-energy X-ray absorptiometry, hematoxylin and eosin staining, and immunohistochemistry were used to evaluate bone changes. TUNEL/DAPI staining assays were used for cell apoptosis detection. Protein expression was determined by western blotting assays. Results A high-fat diet promoted OP development in vivo, and OX-LDL stimulated osteoblast apoptosis in vitro. GEN exhibited protective activities against OX-LDL-induced osteoblast apoptosis by increasing the NRF2 pathway and decreasing the NF-κB pathway. PDTC, an NF-κB inhibitor, could further promote the biological functions of GEN. In contrast, ML385, an NRF2 inhibitor, might eliminate GEN’s protection. Conclusion GEN suppressed OX-LDL-induced osteoblast apoptosis by regulating the NRF2/NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Geniposide suppressed OX-LDL-induced osteoblast apoptosis by regulating the NRF2/NF-κB signaling pathway

Xiao,

Zhang,

et al. 2023

J Orthop Surg Res

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“…IPA was performed as described previously 24 , 25 . Briefly, molecules associated with shorter survival were analyzed by IPA software to search for canonical pathways.…”

Section: Methodsmentioning

confidence: 99%

A new bioinformatics approach identifies overexpression of GRB2 as a poor prognostic biomarker for prostate cancer

Iwata

Sedukhina

Kubota

et al. 2021

Sci Rep

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A subset of prostate cancer displays a poor clinical outcome. Therefore, identifying this poor prognostic subset within clinically aggressive groups (defined as a Gleason score (GS) ≧8) and developing effective treatments are essential if we are to improve prostate cancer survival. Here, we performed a bioinformatics analysis of a TCGA dataset (GS ≧8) to identify pathways upregulated in a prostate cancer cohort with short survival. When conducting bioinformatics analyses, the definition of factors such as “overexpression” and “shorter survival” is vital, as poor definition may lead to mis-estimations. To eliminate this possibility, we defined an expression cutoff value using an algorithm calculated by a Cox regression model, and the hazard ratio for each gene was set so as to identify genes whose expression levels were associated with shorter survival. Next, genes associated with shorter survival were entered into pathway analysis to identify pathways that were altered in a shorter survival cohort. We identified pathways involving upregulation of GRB2. Overexpression of GRB2 was linked to shorter survival in the TCGA dataset, a finding validated by histological examination of biopsy samples taken from the patients for diagnostic purposes. Thus, GRB2 is a novel biomarker that predicts shorter survival of patients with aggressive prostate cancer (GS ≧8).

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“…Currently, the researches of Nrf2 in the central nervous system have become a hot spot (Liu et al, 2019;Shah et al, 2019). NF-κB is a family of dimeric transcription factors made up of five family members, p50 (NF-κB1), RelA (p65), p52 (NF-κB2), c-Rel, and RelB (Oda-Kawashima et al, 2020). Zhong et al (2014) revealed down-regulation of p65 was involved in the potential mechanisms of propofol-induced neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

RTA‐408 protects against propofol‐induced cognitive impairment in neonatal mice via the activation of Nrf2 and the inhibition of NF‐κB p65 nuclear translocation

Zhang

Zhou

2020

Brain and Behavior

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Objective To explore the effect of RTA‐408 on the propofol‐induced cognitive impairment of neonatal mice via regulating Nrf2 and NF‐κB p65 nuclear translocation. Methods C57BL/6 neonatal mice were randomized into intralipid, propofol, vehicle + propofol, and RTA‐408 + propofol groups. The learning and memory ability was inspected by Morries water maze (MWM) test. TUNEL staining was performed to examine the apoptosis of neurons in hippocampus. The gene and protein expressions in hippocampus were detected by immunohistochemistry, qRT‐PCR, or Western blotting. The activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were tested by the corresponding kits. Results Propofol prolonged escape latency of mice, decreased the times of crossing the platform, and shortened the time of staying in the target quadrant, while RTA‐408 treatment improved the above‐mentioned situation. Besides, Nrf2 protein in hippocampus of mice induced by propofol was decreased with the increased NF‐κB p65 nuclear translocation, which was reversed by RTA‐408. Meanwhile, RTA‐408 decreased the apoptosis of neurons accompanying with the down‐regulation of Caspase‐3 and the up‐regulations of neuronal‐specific nuclear protein (NeuN), microtubule‐associated protein 2 (Map2), Ca2+/Calmodulin‐dependent Protein Kinase II (CaMKII), and parvalbumin (PV) immunostaining in hippocampus. Besides, propofol‐induced high levels of proinflammatory cytokines and antioxidase activities in hippocampus were reduced by RTA‐408. Conclusion RTA‐408 improved propofol‐induced cognitive impairment in neonatal mice via enhancing survival of neurons, reducing the apoptosis of hippocampal neurons, mitigating the inflammation and oxidative stress, which may be correlated with the activation of Nrf2 and the inhibition of NF‐κB p65 nuclear translocation.

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NF‐kB signaling in cardiomyocytes is inhibited by sevoflurane and promoted by propofol

Cited by 4 publications

References 31 publications

Geniposide suppressed OX-LDL-induced osteoblast apoptosis by regulating the NRF2/NF-κB signaling pathway

Geniposide suppressed OX-LDL-induced osteoblast apoptosis by regulating the NRF2/NF-κB signaling pathway

A new bioinformatics approach identifies overexpression of GRB2 as a poor prognostic biomarker for prostate cancer

RTA‐408 protects against propofol‐induced cognitive impairment in neonatal mice via the activation of Nrf2 and the inhibition of NF‐κB p65 nuclear translocation

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