The protective effects of dezocine on interleukin-1β-induced inflammation, oxidative stress and apoptosis of human nucleus pulposus cells and the possible mechanisms

Zhu, Fang; Duan, Wei; Zhong, Chao; Ji, Bing; Liu, Xinjun

doi:10.1080/21655979.2021.2017700

Cited by 16 publications

(9 citation statements)

References 48 publications

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“…IL‐1β is one of these pro‐inflammatory factors to activate NF‐κB. The activation of NF‐κB upregulates the release of IL‐1β, IL‐6, 42 and tumor necrosis factor‐α (TNF‐α), 43 which fuels apoptosis 44,45 and inflammation 46,47 . ROS activated by IL‐1β is another pro‐inflammatory factors 48 .…”

Section: Introductionmentioning

confidence: 99%

Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Wang

Qian

Xiao

et al. 2023

Immunity Inflam & Disease

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Background: Interleukin-1β (IL-1β) is a pro-inflammatory cytokine mainly produced by monocytes and macrophages with a wide range of biological effects. Evidence has shown that IL-1β plays a vital role in the process of apoptosis; however, the specific mechanisms, by which IL-1β induces apoptosis, vary due to different cellular and experimental conditions. Therefore, this present reviewstudy aimed to systematically review the association between the molecular mechanisms of IL-1β-induced apoptosis in pathological processes and the role of signaling pathways. This article also sought to briefly investigate the potential of signaling pathway-targeted therapy in the prevention and treatment of disease. Methods: This is a literature review article. The present discourse aim is first to scrutinize and assess the available literature on IL-1β and apoptosis. The relevant studies using the keywords of "IL-1β-induced apoptosis" and "signaling pathways" were searched in the databases of PubMed, Scopus, Google Scholar, and Web of Science. Gathered relevant material, and extracted information was then assessed. Results: IL-1β can induce apoptosis in various types of cells under different external stimuli via the mitochondrial pathway, death receptor pathway and endoplasmic reticulum pathway, and that the different pathways are often interconnected. The NF-KB signaling pathway, p38MAPK, and JNK signaling pathways mainly play a proapoptotic part, and the ERK1/2 pathway has a bidirectional role in regulating apoptosis, while activation of the PI3K-Akt signaling pathway can inhibit apoptosis. Conclusion: This review indicates that IL-1β-induced apoptosis plays an important role in pathogenesis and development of pathology of many inflammatory diseases. Elucidating the role of the signaling pathways will aid the development of targeted therapeutic treatments.

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Section: Introductionmentioning

confidence: 99%

Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Wang

Qian

Xiao

et al. 2023

Immunity Inflam & Disease

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“…As reported, the apoptosis of IL-1β -induced hNPCs can be influenced by multiple factors including higenamine ( 44 ), tyrosol ( 45 ), dezocine ( 46 ), Omentin-1 ( 47 ) and so on. PNS is a traditional Chinese medicine with important clinical value ( 6 ).…”

Section: Discussionmentioning

confidence: 98%

Panax notoginseng saponin reduces IL-1β-stimulated apoptosis and endoplasmic reticulum stress of nucleus pulposus cells by suppressing miR-222-3p

et al. 2022

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Background It is well documented that the malignant biological behaviors of nucleus pulposus cells (NPCs) could trigger intervertebral disc degeneration (IDD). Panax notoginseng saponin (PNS) is a traditional Chinese medicine that inhibits osteoclastogenesis. However, its effects on the phenotypes of NPCs in IDD remains largely unknown. This study sought to examine the role of PNS in IDD and its regulatory mechanism. Methods First, human NPCs (hNPCs) were treated with interleukin-1 beta ( IL-1β ) to induce an IDD cell model. Cell proliferation and apoptosis were estimated by Cell Counting Kit-8 (CCK-8) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. Western blot was employed to examine the levels of proteins related to apoptosis and endoplasmic reticulum (ER) stress. Enzyme-linked immunosorbent assays (ELISAs) were used to test inflammatory factors levels. Immunofluorescence (IF) assays were used to determine the nuclear translocation of nuclear factor-kappa beta ( NF-κB ) p65 . Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect miR-222-3p expression. Results We discovered that PNS enhanced the viability but reduced the apoptosis, inflammation, and ER stress response of IL-1β -induced hNPCs in a concentration-dependent manner. Additionally, PNS significantly reduced miR-222-3p expression in the IL-1β -induced hNPCs. Notably, these PNS effects were reversed by the upregulation of miR-222-3p . Conclusions In summary, PNS appears to facilitate the proliferation and attenuate the apoptosis, inflammatory response, and ER stress response of IL-1β -induced hNPCs by inhibiting miR-222-3p expression. Our findings provide a theoretical basis for a novel drug application in IDD research.

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“…Activated NF-κB also induces the expression of inflammatory factors, such as IL-1β, IL-6, and TNF-α to exacerbate inflammation ( Ma et al, 2020 ). These inflammatory factors also stimulate ROS production to exacerbate oxidative damage ( Zhu et al, 2022 ). A vicious cycle exists between oxidative stress and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis

et al. 2022

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Osteoporosis is a common bone imbalance disease that threatens the health of postmenopausal women. Estrogen deficiency accelerates the aging of women. Oxidative stress damage is regarded as the main pathogenesis of postmenopausal osteoporosis. The accumulation of reactive oxygen species in the bone microenvironment plays a role in osteoblast and osteoclast apoptosis. Improving the oxidative state is essential for the prevention and treatment of postmenopausal osteoporosis. There are three classes of antioxidant defense systems in the body to eliminate free radicals and peroxides including antioxidant substances, antioxidant enzymes, and repair enzymes. In our review, we demonstrated the mechanism of antioxidants and their effect on bone metabolism in detail. We concluded that glutathione/oxidized glutathione (GSH/GSSG) conversion involved the PI3K/Akt-Nrf2/HO-1 signaling pathway and that the antioxidant enzyme-mediated mitochondrial apoptosis pathway of osteoblasts was necessary for the development of postmenopausal osteoporosis. Since the current therapeutic effects of targeting bone cells are not significant, improving the systemic peroxidation state and then regulating bone homeostasis will be a new method for the treatment of postmenopausal osteoporosis.

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The protective effects of dezocine on interleukin-1β-induced inflammation, oxidative stress and apoptosis of human nucleus pulposus cells and the possible mechanisms

Cited by 16 publications

References 48 publications

Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Role of signal transduction pathways in IL‐1β‐induced apoptosis: Pathological and therapeutic aspects

Panax notoginseng saponin reduces IL-1β-stimulated apoptosis and endoplasmic reticulum stress of nucleus pulposus cells by suppressing miR-222-3p

Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis

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