The protective effects of etomidate against interleukin-1β (IL-1β)-induced oxidative stress, extracellular matrix alteration and cellular senescence in chondrocytes

Background: Stress-induced cellular senescence is a perpetual state of cell cycle arrest occurring in proliferating cells in response to stressful conditions. It is believed that oxidative stress plays a unique role in this process. As a reactive chemical compound that can induce oxidative stress, acrylamide is widely applied in several fields. Carvacrol is a liquid phenolic monoterpenoid found in essential oils of some plants and is known for its antioxidant and anticarcinogenic properties. Objectives: The current study aimed to evaluate the effects of carvacrol on oxidative stress and cellular senescence induced by acrylamide in the NIH 3T3 cell line. Methods: NIH 3T3 embryonic fibroblast cells were exposed to different concentrations of acrylamide, carvacrol, and H2O2 in a cell culture medium. The level of β-galactosidase (SA-β-gal) activity, as a marker of cellular senescence, was measured using staining and quantitative assays. Furthermore, to measure oxidative stress parameters, the content of glutathione and lipid peroxidation were determined. Results: Acrylamide could induce premature senescence evident by the elevated lipid peroxidation and SA-β-gal activity and declined cell viability and glutathione. Moreover, carvacrol showed beneficial effects on both acrylamide- and H2O2-induced cellular senescence by significantly reversing or subsiding the effect of oxidative stress and mediating its consequences. Conclusions: It can be concluded that carvacrol has protective effects against oxidative cellular senescence induced by acrylamide in the NIH 3T3 cell line.

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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

Bioengineered ◽

10.1080/21655979.2021.2017700 ◽

2022 ◽

Vol 13 (1) ◽

pp. 1399-1410

Author(s):

Fang Zhu ◽

Wei Duan ◽

Chao Zhong ◽

Bing Ji ◽

Xinjun Liu

Keyword(s):

Oxidative Stress ◽

Nucleus Pulposus ◽

Interleukin 1Β ◽

Protective Effects ◽

Nucleus Pulposus Cells

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Matrix Metalloproteinases and Arterial Hypertension: Role of Oxidative Stress and Nitric Oxide in Vascular Functional and Structural Alterations

Biomolecules ◽

10.3390/biom11040585 ◽

2021 ◽

Vol 11 (4) ◽

pp. 585

Author(s):

Alejandro F. Prado ◽

Rose I. M. Batista ◽

Jose E. Tanus-Santos ◽

Raquel F. Gerlach

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Extracellular Matrix ◽

Vascular Function ◽

Vascular Dysfunction ◽

Protective Effects ◽

Pathophysiological Mechanisms ◽

Emerging Therapies ◽

Extracellular Matrix Components ◽

Matrix Components

Various pathophysiological mechanisms have been implicated in hypertension, but those resulting in vascular dysfunction and remodeling are critical and may help to identify critical pharmacological targets. This mini-review article focuses on central mechanisms contributing to the vascular dysfunction and remodeling of hypertension, increased oxidative stress and impaired nitric oxide (NO) bioavailability, which enhance vascular matrix metalloproteinase (MMP) activity. The relationship between NO, MMP and oxidative stress culminating in the vascular alterations of hypertension is examined. While the alterations of hypertension are not fully attributable to these pathophysiological mechanisms, there is strong evidence that such mechanisms play critical roles in increasing vascular MMP expression and activity, thus resulting in abnormal degradation of extracellular matrix components, receptors, peptides, and intracellular proteins involved in the regulation of vascular function and structure. Imbalanced vascular MMP activity promotes vasoconstriction and impairs vasodilation, stimulating vascular smooth muscle cells (VSMC) to switch from contractile to synthetic phenotypes, thus facilitating cell growth or migration, which is associated with the deposition of extracellular matrix components. Finally, the protective effects of MMP inhibitors, antioxidants and drugs that enhance vascular NO activity are briefly discussed. Newly emerging therapies that address these essential mechanisms may offer significant advantages to prevent vascular remodeling in hypertensive patients.

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Cardamonin Alleviates Oxidative Stress, Cell Apoptosis Level and Extracellular Matrix Degradation by Inhibiting NF-kb in ILβ-1 -Induced Chondrocytes

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2020.2299 ◽

2020 ◽

Vol 10 (5) ◽

pp. 589-595

Author(s):

Chongxin Li ◽

Wei Zeng

Keyword(s):

Oxidative Stress ◽

Extracellular Matrix ◽

Cell Apoptosis ◽

Cell Model ◽

Joint Disease ◽

Protective Effects ◽

Matrix Degradation ◽

Extracellular Matrix Degradation ◽

Apoptosis Detection ◽

Apoptosis Level

Currently, osteoarthritis as degenerative chronic joint disease remains unsolved and finding the effective targeting therapeutic agent is pressing. Therefore, in this research, we aimed to investigate the effects of cardamonin, the NF-kb inhibitor, in cell model of osteoarthritis. IL-1β that induced chondrocytes served as the cell model of osteoarthritis. The cells were divided into control, IL-1β and IL-1+ cardamonin groups. Western blot assays were performed for assessment of protein expression level and PCR for gene level. Flow cytometry was used for cell apoptosis detection. MDA, LDH SOD and ROS were detected by corresponding kits. The NF-kb was activated by IL-1. The entrance of NF-kb into cell nucleus was inhibited by cardamonin in IL-1β-induced cells. The MDA, LDH and ROS were increased by IL-1β and SOD was down-regulated by IL-1β. This effect of IL-1β was reduced by cardamonin. The cell apoptosis and pro-apoptosis proteins were increased and BCl-2 was down-regulated in IL-1β-induced cells. After cardamonin treatment, this effect was inhibited. The extracellular matrix degradation as well as the relative degradation enzymes was elevated by IL-1β, and this effect was further inhibited by cardamonin as well. Cardamonin exerted protective effects via alleviating oxidative stress, cell apoptosis level and extracellular matrix degradation by inhibiting NF-kb in IL-1β-induced chondrocytes. Cardamonin as NF-kb inhibitor was a promising drug for therapy of osteoarthritis.

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Interleukin-1β Drives Cellular Senescence of Rat Astrocytes Induced by Oligomerized Amyloid β Peptide and Oxidative Stress

Frontiers in Neurology ◽

10.3389/fneur.2020.00929 ◽

2020 ◽

Vol 11 ◽

Author(s):

Dongsheng Shang ◽

Yin Hong ◽

Wangwang Xie ◽

Zhigang Tu ◽

Jun Xu

Keyword(s):

Oxidative Stress ◽

Cellular Senescence ◽

Amyloid Β ◽

Interleukin 1Β ◽

Amyloid Β Peptide ◽

Rat Astrocytes ◽

And Oxidative Stress

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Protective effects of pyrroloquinoline quinone against oxidative stress-induced cellular senescence and inflammation in human renal tubular epithelial cells via Keap1/Nrf2 signaling pathway

International Immunopharmacology ◽

10.1016/j.intimp.2019.04.040 ◽

2019 ◽

Vol 72 ◽

pp. 445-453 ◽

Cited By ~ 6

Author(s):

Ziqiang Wang ◽

Ning Han ◽

Kunxiao Zhao ◽

Ying Li ◽

Yanqing Chi ◽

...

Keyword(s):

Oxidative Stress ◽

Epithelial Cells ◽

Signaling Pathway ◽

Cellular Senescence ◽

Pyrroloquinoline Quinone ◽

Protective Effects ◽

Tubular Epithelial Cells ◽

Renal Tubular Epithelial Cells ◽

Nrf2 Signaling Pathway ◽

Renal Tubular

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Anti-degenerative effect of melatonin on intervertebral disc: protective contribution against inflammation, oxidative stress, apoptosis, and autophagy

Current Drug Targets ◽

10.2174/1389450123666220114151654 ◽

2022 ◽

Vol 23 ◽

Author(s):

Karim Hemati ◽

Mohammad Hossein Pourhanifeh ◽

Iman Fatemi ◽

Azam Hosseinzadeh ◽

Saeed Mehrzadi

Keyword(s):

Oxidative Stress ◽

Extracellular Matrix ◽

Back Pain ◽

Intervertebral Disc ◽

Lower Back Pain ◽

Cartilage Tissue ◽

Protective Effects ◽

Lower Back ◽

Collagen Ii ◽

Ivd Degeneration

Abstract: Intervertebral disc (IVD) degeneration is a leading cause of lower back pain. Although the etiology of IVD degeneration (IVDD) is unclear, excessive oxidative stress, inflammation and apoptosis and disruption of autophagy play important role in the pathogenesis of IVDD. Therefore, finding a solution to mitigate these processes could stop or reduce the development of IVDD. Melatonin, a powerful antioxidant, plays an important role in regulating cartilage tissue hemostasis. Melatonin inhibits destruction of extracellular matrix (ECM) of disc. Melatonin preserves ECM contents including sox-9, aggrecan, and collagen II through inhibiting matrix degeneration enzymes such as MMP-13. These protective effects may be mediated by the inhibition of oxidative stress, inflammation and apoptosis, and regulation of autophagy in IVD cells.

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Link between increased cellular senescence and extracellular matrix changes in COPD

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00028.2020 ◽

2020 ◽

Vol 319 (1) ◽

pp. L48-L60 ◽

Cited By ~ 3

Author(s):

Roy R. Woldhuis ◽

Maaike de Vries ◽

Wim Timens ◽

Maarten van den Berge ◽

Marco Demaria ◽

...

Keyword(s):

Oxidative Stress ◽

Extracellular Matrix ◽

Dna Damage ◽

Lung Tissue ◽

Cellular Senescence ◽

Accelerated Aging ◽

Lung Fibroblasts ◽

Copd Patients ◽

And Oxidative Stress ◽

P16 Expression

Chronic obstructive pulmonary disease (COPD) is associated with features of accelerated aging, including cellular senescence, DNA damage, oxidative stress, and extracellular matrix (ECM) changes. We propose that these features are particularly apparent in patients with severe, early-onset (SEO)-COPD. Whether fibroblasts from COPD patients display features of accelerated aging and whether this is also present in relatively young SEO-COPD patients is unknown. Therefore, we aimed to determine markers of aging in (SEO)-COPD-derived lung fibroblasts and investigate the impact on ECM. Aging hallmarks and ECM markers were analyzed in lung fibroblasts from SEO-COPD and older COPD patients and compared with fibroblasts from matched non-COPD groups ( n = 9–11 per group), both at normal culture conditions and upon Paraquat-induced senescence. COPD-related differences in senescence and ECM expression were validated in lung tissue. Higher levels of cellular senescence, including senescence-associated β-galactosidase (SA-β-gal)-positive cells (19% for COPD vs. 13% for control) and p16 expression, DNA damage (γ-H2A.X-positive nuclei), and oxidative stress ( MGST1) were detected in COPD compared with control-derived fibroblasts. Most effects were also different in SEO-COPD, with SA-β-gal-positive cells only being significant in SEO-COPD vs. matched controls. Lower decorin expression in COPD-derived fibroblasts correlated with higher p16 expression, and this association was confirmed in lung tissue. Paraquat treatment induced cellular senescence along with clear changes in ECM expression, including decorin. Fibroblasts from COPD patients, including SEO-COPD, display higher levels of cellular senescence, DNA damage, and oxidative stress. The association between cellular senescence and ECM expression changes may suggest a link between accelerated aging and ECM dysregulation in COPD.

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