scholarly journals Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway

2020 ◽  
Author(s):  
Yin GUAN ◽  
Xiaoqian ZHAO ◽  
Weiwei LIU ◽  
Yue Wang
Keyword(s):  
Cell Proliferation ◽  
Caspase 3 ◽  
Inflammatory Factors ◽  
Tunel Staining ◽  
Dependent Manner ◽  
Protective Effects ◽  
Tnf Α ◽  
Apoptosis And Inflammation ◽  
Dose Dependent ◽  
Anti Inflammation

Abstract Objective: Galuteolin (Galu) is a substance extracted and purified from honeysuckle. The purpose of this study was to explore the effects of Galu on the TNF-α-induced RA-FLS cells (synoviocytes) and reveal its potential molecular mechanism from the perspectives of anti-apoptosis and anti-inflammation.Methods: After TNF-α stimulation, cell proliferation of RA-FLS was assessed by CCK-8 assay. TUNEL staining was used to detect the apoptosis. Western Blot was used to detect the expressions of Iκκβ, p-p65, p65, p-IκB, IκB, Cleaved-caspase3, Caspase-3, Bcl-2, and Bax. HO-1 were determined by RT-PCR. The contents of pro-inflammatory cytokines IL-1β, IL-6, IL-8 and MMP-1 were determined by ELISA.Results: Galu significantly suppressed cell proliferation in a dose-dependent manner. Additionally, Galu obviously promote cell apoptosis rate of RA-FLS cells and elevated the expression levels of HO-1, caspase-3 and Bax, while reduced the expression level of Bcl-2. Furthermore, Galu apparently inhibited the levels of Iκκβ, p-p65 and p-IκB. Moreover, Galu also significantly reduced the levels of pro-inflammatory factors IL-1β, IL-6, IL-8 and MMP-1 in RA-FLS cells. Conclusion: Galuteolin exerts protective effects against TNF-α-induced RA-FLS cells by inhibiting apoptosis and inflammation, which can guide the clinical use of rheumatoid arthritis.

scholarly journals Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Yin Guan ◽  
Xiaoqian Zhao ◽  
Weiwei Liu ◽  
Yue Wang
Keyword(s):  
Cell Proliferation ◽  
Caspase 3 ◽  
Inflammatory Factors ◽  
Tunel Staining ◽  
Dependent Manner ◽  
Protective Effects ◽  
Tnf Α ◽  
Apoptosis And Inflammation ◽  
Dose Dependent ◽  
Anti Inflammation

Abstract Objective Galuteolin (Galu) is a substance extracted and purified from honeysuckle. The purpose of this study was to explore the effects of Galu on the TNF-α-induced RA-FLS cells (synoviocytes) and reveal its potential molecular mechanism from the perspectives of anti-apoptosis and anti-inflammation. Methods After TNF-α stimulation, cell proliferation of RA-FLS was assessed by CCK-8 assay. TUNEL staining was used to detect the apoptosis. Western blot was used to detect the expressions of Iκκβ, p-p65, p65, p-IκB, IκB, Cleaved-caspase3, Caspase-3, Bcl-2, and Bax. HO-1 were determined by RT-PCR. The contents of pro-inflammatory cytokines IL-1β, IL-6, IL-8, and MMP-1 were determined by ELISA. Results Galu significantly suppressed cell proliferation in a dose-dependent manner. Additionally, Galu obviously promotes cell apoptosis rate of RA-FLS cells and elevated the expression levels of HO-1, caspase-3, and Bax, while reducing the expression level of Bcl-2. Furthermore, Galu apparently inhibited the levels of Iκκβ, p-p65, and p-IκB. Moreover, Galu also significantly reduced the levels of pro-inflammatory factors IL-1β, IL-6, IL-8, and MMP-1 in RA-FLS cells. Conclusion Galuteolin exerts protective effects against TNF-α-induced RA-FLS cells by inhibiting apoptosis and inflammation, which can guide the clinical use of rheumatoid arthritis.

MK886 Induced Apoptosis in HL-60 Cells Via Inhibition mPGES-1 Expression and Down-Regulation Prostaglandin E2 Synthesize.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4824-4824
Author(s):  
Yiqing Li ◽  
Songmei Yin ◽  
Shuangfeng Xie ◽  
Danian Nie ◽  
Liping Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Prostaglandin E2 ◽  
Cell Line ◽  
Caspase 3 ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Dependent Manner ◽  
Pge2 Synthesis ◽  
Dose Dependent

Abstract Abstract 4824 Recent studies have shown that prostaglandin E2 (PGE2) may play a key role in the tumorigenesis and tumor development. Membrane-bound prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that acts downstream of cyclooxygenase (COX) and specifically catalyzes the conversion of prostaglandin H2 (PGH2) to PGE2, was over-expression in a variety of solid tumor cells and tissues such as nonsmall-cell lung cancer, colon carcinoma, gastric carcinoma and breast cancer. MK886, a small molecular inhibitor, is a reasonable potency as an inhibitor of mPGES-1 in vitro experiment. In this study, we examined effects of MK886 on expression of mPGES-1 and PGE2 synthesis in human acute myeloid leukemia cell line (HL-60), observed cell proliferation and apoptosis after 24-h treatment with MK886, and tried to explore the possible mechanisms by checking some protein belong AKT cell singling pathway such as P-AKT, Bax and Bcl-2. We found that the expression levels of mPGES-1 mRNA and protein were higher in HL-60 cells than in normal mononuclearcells (MNC). MK886 inhibited mPGES-1 mRNA and protein expression and reduced PGE2 secretion in HL-60 cells in a dose-dependent manner. The cell proliferation was inhibited and the IC50 was 132.16μmol/L. With the increase of MK886 concentration, the cell apoptosis rate assayed by flow cytometry increased and the apparent apoptotic bodies increased when staining by Hoechst 33258. After treated with MK886 for 24h, protein was extracted and assayed by western blot. The results showed that the expression levels of P-AKT, Bcl-2 and c-myc decreased while the Bax protein expression increased in a dose-dependent manner. The caspase-3 activity, determined by colorimetric detection, also increased dose-dependently. These results indicated that mPGES-1 over-expressed in leukemia cell line HL-60, MK886 could induce apoptosis in HL-60 cells via reducing mPGES-1 expression and PGE2 synthesis dose-dependently, thereby regulate the AKT pathway including Bcl-2 family and the activity of caspase-3. It suggested that mPGES-1 inhibitor might emerge as an important therapeutic tool for leukemia treatment. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Hyperoside Protects HK-2 Cells Against High Glucose-Induced Apoptosis and Inflammation via the miR-499a-5p/NRIP1 Pathway

2021 ◽  
Vol 27 ◽  
Author(s):  
Jingbo Zhou ◽  
Shu Zhang ◽  
Xinyi Sun ◽  
Yan Lou ◽  
Jiangyi Yu
Keyword(s):  
Inflammatory Response ◽  
High Glucose ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Protective Effects ◽  
Human Papillomavirus 16 ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
Dose Dependent

Hyperoside, a flavonol glycoside, is derived from plants of the genera Hypericum and Crataegus. Recent studies have indicated the anti-apoptotic and anti-inflammatory roles of hyperoside. The present study was designed to measure the effects of hyperoside on high glucose (HG)-treated HK-2 cells. HK-2 is a human papillomavirus 16 transformed cell line and can be used as a model for normal tubular cell. Cell apoptosis was examined by TUNEL assays and flow cytometry analysis. Inflammatory response was detected by Enzyme linked immunosorbent assay kits. Western blotting was applied to detect protein levels of apoptosis-related genes and inflammatory cytokines. Mechanistical assays including luciferase reporter and RNA pull down assays were applied to detect the binding relationship between molecules. We identified that hyperoside protected HK-2 cells against HG-induced apoptosis and inflammation. Moreover, miR-499a-5p was upregulated by hyperoside in a dose dependent manner. MiR-499a-5p inhibition rescued the suppressive effects of hyperoside on apoptosis and inflammation of HG-treated HK-2 cells. Furthermore, miR-499a-5p targeted NRIP1 to inhibit its mRNA expression, and further suppressed its translation. NRIP1 was downregulated by hyperoside in a dose dependent manner. Finally, rescue assays indicated that miR-499a-5p inhibition rescued the protective effects of hyperoside on apoptosis and inflammatory response of HK-2 cells by NRIP1. In conclusion, our findings revealed that hyperoside alleviates HG-induced apoptosis and inflammatory response of HK-2 cells by the miR-499a-5p/NRIP1 axis.

scholarly journals Tetramethylpyrazine protects Schwann cells from ischemia-like injury and increases cell survival in cold ischemic rat nerves

2015 ◽  
Vol 51 (1) ◽  
pp. 127-141
Author(s):  
Ming-Ming Yang ◽  
Wei Huang ◽  
Dian-Ming Jiang
Keyword(s):  
Cell Viability ◽  
Cell Survival ◽  
Schwann Cells ◽  
Caspase 3 ◽  
Chinese Herb ◽  
Dependent Manner ◽  
Protective Effects ◽  
Injury Model ◽  
Nerve Model ◽  
Dose Dependent

Tetramethylpyrazine (TMP), a major active ingredient of Ligusticum wallichi Franchat extract (a Chinese herb), exhibits neuroprotective properties in ischemia. In this study, we assessed its protective effects on Schwann cells (SCs) by culturing them in the presence of oxygen glucose deprivation (OGD) conditions and measuring cell survival in cold ischemic rat nerves. In the OGD-induced ischemic injury model of SCs, we demonstrated that TMP treatment not only reduced OGD-induced cell viability losses, cell death, and apoptosis of SCs in a dose-dependent manner, and inhibited LDH release, but also suppressed OGD-induced downregulation of Bcl-2 and upregulation of Bax and caspase-3, as well as inhibited the consequent activation of caspase-3. In the cold ischemic nerve model, we found that prolonged cold ischemic exposure for four weeks was markedly associated with the absence of SCs, a decrease in cell viability, and apoptosis in preserved nerve segments incubated in University of Wisconsin solution (UWS) alone. However, TMP attenuated nerve segment damage by preserving SCs and antagonizing the decrease in nerve fiber viability and increase in TUNEL-positive cells in a dose-dependent manner. Collectively, our results indicate that TMP not only provides protective effects in an ischemia-like injury model of cultured rat SCs by regulating Bcl-2, Bax, and caspase-3, but also increases cell survival and suppresses apoptosis in the cold ischemic nerve model after prolonged ischemic exposure for four weeks. Therefore, TMP may be a novel and effective therapeutic strategy for preventing peripheral nervous system ischemic diseases and improving peripheral nerve storage.

Madhuca longifolia embedded silver nanoparticles attenuates diethylnitrosamine (DEN) -induced renal cancer via regulating oxidative stress

2020 ◽  
Vol 17 ◽  
Author(s):  
Deepika Singh ◽  
Ekta Yadav ◽  
Vikas Kumar ◽  
Amita Verma
Keyword(s):  
Silver Nanoparticles ◽  
Renal Cancer ◽  
Safety Concern ◽  
Treated Group ◽  
Dependent Manner ◽  
Protective Effects ◽  
Antineoplastic Effect ◽  
Tnf Α ◽  
Madhuca Longifolia ◽  
Dose Dependent

Objective: Madhuca longifolia has been used for the treatment of renal cancer. Therefore, the current study describes the protective effects of biofabricated silver nanoparticles (MLAgNPs) using Madhuca longifolia aqueous leaves extract against diethylnitrosamine (DEN) induced renal cell carcinoma (RCC) in rats. Methods: Animals were categorized into five groups and treated with doses of silver nanoparticles for 16 weeks. Antineoplastic effect in renal cancer was dose dependent to control the macroscopical variations when compared to DEN induced group. Significant changes were observed in biochemical parameters and dose graded improvement in the level of antioxidants parameters were accountable for its protective nature. Result: Silver nanoparticles in dose dependent manner was effective to modify the raised levels of pro-inflammatory cytokines and inflammatory mediators during renal cancer. Alteration in renal histopathology were also detected in the silver nanoparticles treated group, which show its safety concern. Biofabricated silver nanoparticles (MLAgNPs) using Madhuca longifolia can convey significant chemo-protective effect against renal cancer by suppressing the IL-6, TNF-α and IL-1β by nuclear factor-kappa B (NF-κB) pathway. Conclusion: Our outcomes implicates that biofabricated MLAgNPs exhibited a chemoprotective potential in the prevention and intervention of RCC.

Berbamine-Induced Apoptosis in Human Leukemia K562 Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4234-4234
Author(s):  
Xiaoying Zhao ◽  
Lei Xu ◽  
Dong Wu ◽  
Rongzhen Xu
Keyword(s):  
Flow Cytometry ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
K562 Cells ◽  
Human Leukemia ◽  
Dependent Manner ◽  
Flow Cytometry Assay ◽  
Transcript Levels ◽  
Induced Apoptosis ◽  
Dose Dependent

Abstract Purpose: To investigate apoptosis-inducing effects of Berbamine on human leukemia cells and to explore the underlying mechanism. Materials and methods: Berbamine was dissolved in 0.9% sodium chloride to an initial concentration of 1mg/ml and subsequently diluted to desired concentrations with cell culture medium. MTT was used to examine the effect of Berbamine on cell proliferation of K562 cells. Characteristic cellular morphological changes were used as indicators of apoptosis in K562 cells while the rate of apoptosis was measured by flow cytometry assay. Expression levels of apoptosis related genes bcl-2 and bax were determined by RT-PCR and the levels of bcr/abl were evaluated by nested-PCR. Levels of Caspase 3 were measured by flow cytometry assay. Results: Berbamine inhibited the cell proliferation significantly and in a dose-dependent manner in tested K562 cells. Its IC50 value was 5.23ug/ml. As determined by morphological observations and flow cytometry assay, Berbamine was able to induce apoptosis of K562 cells within 6 hours. The apoptosis rate of K562 was also dose-dependent. Steady-state transcript levels of bcr/abl decreased dramatically (half-quantity ratio from 1.284 to 0.506 within 72 hours following 8mg/ml Berbamine treatment. On the other hand, the protein levels of Caspase 3 surged from 18.36% to 38.25% (p<0.001) within 24 hours after treatment of 12mg/ml Berbamine. During the same period, no changes of bcl-2 or bax transcript levels were detected in the cells that were treated with 8mg/ml Berbamine. Conclusions: Our results suggest that Berbamine is a potent inhibitor of cell proliferation and a strong inducer of apoptosis in human K562 cells. The Berbamine-induced apoptosis pathway involves down regulation of bcr/abl and up regulation of Caspase 3 expressions. Neither bcl-2 nor bax plays substantial roles in Berbamine-induced K562 cell apoptosis.

Oroxylin A Shows Protective Effects on Biological Activity of Lipopolysaccharide Treated Human Periodontal Ligament Stem Cells

2019 ◽  
Vol 9 (10) ◽  
pp. 1362-1368
Author(s):  
Ting Wang ◽  
Xinqiang Liu ◽  
Chunmiao Jiang ◽  
Dapeng Ren ◽  
Yuli Gao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Biological Activity ◽  
Periodontal Ligament ◽  
Time Dependent ◽  
Dependent Manner ◽  
Protective Effects ◽  
Oroxylin A ◽  
Periodontal Ligament Stem Cells ◽  
Dose Dependent

The abnormal proliferation and apoptosis of human periodontal ligament stem cells (hPDLSCs) serves a crucial role in the development of periodontitis. Oroxylin A has shown protective effects in a variety of inflammatory diseases. The present study was aimed to investigate the effects of oroxylin A on lipopolysaccharide (LPS) treated hPDLSCs. In the present study, cells were exposed to different concentrations (10, 20, 40 uM) of oroxylin A for 24 h or 48 h, co-treated with LPS. The cell proliferation capacity was assessed using cell counting kit-8 (CCK-8), and the cell apoptosis was evaluated by flow cytometry. The Ki67 expression was measured using immunofluorescence and NO production was detected by enzyme linked immunosorbent assay (ELISA) respectively. Western blot analyses were used to investigate the level of cell proliferation related proteins (PCNA, CDK2 and p21) as well as NF-κB, I-κBα and downstream molecules iNOS, IL-6 and TNF-α. The results demonstrated that oroxylin A increased cell survival of LPS treated hPDLSCs in a dose-dependent and time-dependent manner. In addition, oroxylin A treatment inhibited cell apoptosis in hPDLSCs. Furthermore, the levels of NO, NF-κB, iNOS, IL-6 and TNF-α were significantly reduced. And the expression of Ki67, I-κBα, PCNA and CDK2 were significantly increased. Taken together, these findings indicate that oroxylin A promote proliferation and suppress apoptosis in a dose-dependent and time-dependent manner. Oroxylin A may affects LPS induced biological activity via inhibiting NF-κB activation and proinflammatory cytokines expression in hPDLSCs.

scholarly journals Protective Effects of Methane-Rich Saline on Rats with Lipopolysaccharide-Induced Acute Lung Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Aijun Sun ◽  
Weiheng Wang ◽  
Xiaojian Ye ◽  
Yang Wang ◽  
Xiangqun Yang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Caspase 3 ◽  
Interleukin 1 ◽  
Oxygenation Index ◽  
Inflammatory Factors ◽  
Tunel Staining ◽  
Protective Effects ◽  
Novel Therapy ◽  
Anti Inflammatory

Objective. The aim of this research is to evaluate the protective effects of methane-rich saline (MS) on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) and investigate its potential antioxidative, anti-inflammatory, and antiapoptotic activities. Methods. LPS-induced (20 mg/kg) ALI rats were injected with MS (2 ml/kg and 20 ml/kg) before the initiation of LPS induction. Survival rate was determined until 96 h after LPS was induced. Lung injury was assayed by oxygenation index, lung permeability index (LPI), wet-to-dry weight (W/D), and histology. The cells in the bronchoalveolar lavage fluid (BALF) were counted. Oxidative stress was examined by the level of malondialdehyde (MDA) and superoxide dismutase (SOD). Inflammatory factors including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in BALF were determined by ELISA. Lung tissue apoptosis was detected by TUNEL staining and western blotting of caspase-3. Results. It was found that methane significantly prolonged the rat survival, decreased the lung W/D ratio and the content of the inflammatory factors, and reduced the amount of caspase-3 and apoptotic index. In addition, MS increased the level of SOD and decreased the level of MDA significantly. Conclusions. MS protects the LPS-challenged ALI via antioxidative, anti-inflammatory, and antiapoptotic effect, which may prove to be a novel therapy for the clinical management of ALI.

Anthocyanins Extracted from Chinese Blueberry and its Anticancer Effects on HepG2 Cells

2014 ◽  
Vol 887-888 ◽  
pp. 592-595 ◽  
Author(s):  
Ya Wei Li ◽  
Dan Wang ◽  
Xiao Guang Li ◽  
Ying Jin
Keyword(s):  
Cell Proliferation ◽  
Treatment Group ◽  
Liver Cancer ◽  
Western Blotting ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Dependent Manner ◽  
Anticancer Effects ◽  
Proliferation And Apoptosis ◽  
Dose Dependent

Recently studies have demonstrated that anthocyanins from blueberry have anticancer effects. Here, HepG2 cells were treated with anthocyanins (200、400、600、800 and 1000 μg/ml) for 48h, the effects on cell proliferation and apoptosis were investigated. The results suggested that anthocyanins can inhibit the proliferation of HepG2 cells in a dose-dependent manner. The activity of caspase-3 was increased in the anthocyanins treatment group. Moreover, results of Western blotting shown that the expression of Caspase-3 protein increased significantly in the treatment group. Taken together, our data suggest that anthocyanins could be developed as an agent against liver cancer.

scholarly journals Resveratrol attenuates mechanical compression-induced nucleus pulposus cell apoptosis through regulating the ERK1/2 signaling pathway in a disc organ culture

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Zhiwen Zhang ◽  
Feng Wen ◽  
Chengjian He ◽  
Jun Yu
Keyword(s):  
Organ Culture ◽  
Nucleus Pulposus ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Dependent Manner ◽  
Protective Effects ◽  
Mechanical Compression ◽  
High Magnitude ◽  
Regulated Expression ◽  
Dose Dependent

Background: Nucleus pulposus (NP) cell apoptosis is a typical feature within the degenerative disc. High magnitude compression significantly promotes NP cell apoptosis. Several studies have indicated that resveratrol has protective effects on disc cell’s normal biology. Objective: The present study aims to investigate whether resveratrol can attenuate mechanical overloading-induced NP cell apoptosis in a disc organ culture. Methods: Isolated porcine discs were cultured in culture chambers of a mechanically active perfusion bioreactor and subjected to a relatively high magnitude compression (1.3 MPa at a frequency of 1.0 Hz for 2 h once per day) for 7 days. Different concentrations (50 and 100 μM) of resveratrol were added into the culture medium to observe the protective effects of resveratrol against NP cell apoptosis under mechanical compression. The noncompressed discs were used as controls. Results: Similar with the previous studies, this high magnitude compression significantly promoted NP cell apoptosis, reflected by the increased number of terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining-positive NP cells and enzyme (caspase-9 and caspase-3) activity, the up-regulated expression of proapoptotic molecules (Bax and caspase-3/cleaved caspase-3), and down-regulated expression of antiapoptotic molecule (Bcl-2). However, resveratrol partly attenuated NP cell apoptosis under this high magnitude compression in a dose-dependent manner. Additionally, though the ERK1/2 pathway was significantly activated in the mechanical compression group, resveratrol partly attenuated activation of the ERK1/2 pathway under mechanical compression in a dose-dependent manner. Conclusion: Resveratrol attenuates mechanical overloading-induced NP cell apoptosis in a dose-dependent manner, and inhibiting activation of the ERK1/2 pathway may be one potential mechanism behind this regulatory process.

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