scholarly journals Protective effects of theaflavins and epigallocatechin gallate against ZnO-NP-induced apoptosis in rat tracheal epithelial cells

2021 ◽  
Author(s):  
Xiaodong Shan ◽  
Feifei Chen ◽  
Huikang Lin ◽  
Hangjun Zhang ◽  
Yuchi Zhong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Caspase 3 ◽  
Epigallocatechin Gallate ◽  
Protective Effects ◽  
Zno Nps ◽  
Tracheal Epithelial Cells ◽  
Inflammatory Chemokines ◽  
Tracheal Epithelial ◽  
Induced Apoptosis ◽  
Factor Α

Abstract Zinc oxide nanoparticles (ZnO-NPs) can affect human health primarily via inhalation. This study evaluated the protective effects of theaflavins (TFs) and epigallocatechin gallate (EGCG) against ZnO-NP-induced cytotoxicity in rat tracheal epithelial (RTE) cells. After exposure to ZnO-NPs (100 µg/L), treatment with TFs and EGCG (10, 100 and 1000 µg/L) significantly inhibited the levels of reactive oxygen species (ROS), and the content of malondialdehyde (MDA). Treatment also alleviated apoptosis induced by oxidative stress, which was achieved by inhibiting cytochrome C (CytoC) and Caspase 3/8/9 mRNA expression. Upon treatment with the highest concentrations of TFs and EGCG (1000 µg/L), CytoC gene expression was downregulated by 59.10% and 77.27%, Caspase 3 gene expression by 50.03% and 60.01%, Caspase 8 gene expression by 45.11% and 55.57%, and Caspase 9 gene expression by 51.33% and 66.67%. In addition, about the interleukin family as interleukin 1β (IL-1β) and interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and the other inflammatory chemokines like C-C motif chemokine 2 (CCL2), C-X-C motif chemokine 8 (CXCL8) were upregulated in RTE cells in the presence of ZnO-NPs. All factors were gradually rescued after the addition of TFs and EGCG. These results showed that TFs and EGCG could effectively protect RTE cells from oxidative damage induced by ZnO-NPs through antiapoptotic and antioxidant effects.

Role of soluble metals in oil fly ash-induced airway epithelial injury and cytokine gene expression

1999 ◽  
Vol 277 (3) ◽  
pp. L498-L510 ◽  
Author(s):  
Janice A. Dye ◽  
Kenneth B. Adler ◽  
Judy H. Richards ◽  
Kevin L. Dreher
Keyword(s):  
Gene Expression ◽  
Fly Ash ◽  
Dependent Manner ◽  
Airway Epithelial ◽  
Tracheal Epithelial Cells ◽  
Inflammatory Protein ◽  
Tracheal Epithelial ◽  
Oil Fly Ash ◽  
Dose Dependent ◽  
Macrophage Inflammatory Protein

Particulate matter (PM) metal content and bioavailability have been hypothesized to play a role in the health effects epidemiologically associated with PM exposure, in particular that associated with emission source PM. Using rat tracheal epithelial cells in primary culture, the present study compared and contrasted the acute airway epithelial effects of an emission source particle, residual oil fly ash (ROFA), with that of its principal constitutive transition metals, namely iron, nickel, and vanadium. Over a 24-h period, exposure to ROFA, vanadium, or nickel plus vanadium, but not to iron or nickel, resulted in increased epithelial permeability, decreased cellular glutathione, cell detachment, and lytic cell injury. Treatment of vanadium-exposed cells with buthionine sulfoximine further increased cytotoxicity. Conversely, treatment with the radical scavenger dimethylthiourea inhibited the effects in a dose-dependent manner. RT-PCR analysis of RNA isolated from ROFA-exposed rat tracheal epithelial cells demonstrated significant macrophage inflammatory protein-2 and interleukin-6 gene expression as early as 6 h after exposure, whereas gene expression of inducible nitric oxide synthase was maximally increased 24 h postexposure. Again, vanadium (not nickel) appeared to be mediating the effects of ROFA on gene expression. Treatment with dimethylthiourea inhibited both ROFA- and vanadium-induced gene expression in a dose-dependent manner. Corresponding effects were observed in interleukin-6 and macrophage inflammatory protein-2 synthesis. In summary, generation of an oxidative stress was critical to induction of the ROFA- or vanadium-induced effects on airway epithelial gene expression, cytokine production, and cytotoxicity.

Hexarelin protects rat cardiomyocytes from angiotensin II-induced apoptosis in vitro

2004 ◽  
Vol 286 (3) ◽  
pp. H1063-H1069 ◽  
Author(s):  
Jin-Jiang Pang ◽  
Rong-Kun Xu ◽  
Xiang-Bin Xu ◽  
Ji-Min Cao ◽  
Chao Ni ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Caspase 3 ◽  
Cardiomyocyte Apoptosis ◽  
Protective Effects ◽  
Ang Ii ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Rat Cardiomyocytes ◽  
Induced Apoptosis

Loss of cardiomyocytes by apoptosis is proposed to cause heart failure. Angiotensin II (ANG II), an important neurohormonal factor during heart failure, can induce cardiomyocyte apoptosis. Inasmuch as hexarelin has been reported to have protective effects in this process, we examined whether hexarelin can prevent cardiomyocytes from ANG II-induced cell death. Cultured cardiomyocytes from neonatal rats were stimulated with ANG II. Apoptosis was evaluated using fluorescence microscopy, TdT-mediated dUTP nick-end labeling (TUNEL) method, flow cytometry, DNA laddering, and analysis of cell viability by (3,4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). It was found that incubation with 0.1 μmol/l ANG II for 48 h increased cardiomyocyte apoptosis. Administration of 0.1 μmol/l hexarelin significantly decreased this ANG II-induced apoptosis and DNA fragmentation and increased myocyte viability. To further investigate the underlying mechanisms, caspase-3 activity assay and mRNA expression of Bax, Bcl-2, and growth hormone secretagogue receptor (GHS-R; the supposed hexarelin binding site) were examined. GHS-R mRNA was abundantly expressed in cardiomyocytes and was upregulated after administration of hexarelin. These results suggest that hexarelin abates cardiomyocytes from ANG II-induced apoptosis possibly via inhibiting the increased caspase-3 activity and Bax expression induced by ANG II and by increasing the expression of Bcl-2, which is depressed by ANG II. Whether the upregulated expression of GHS-R induced by hexarelin is associated with this antiapoptotic effect deserves further investigation.

scholarly journals Matrix Protein and Another Viral Component Contribute to Induction of Apoptosis in Cells Infected with Vesicular Stomatitis Virus

2001 ◽  
Vol 75 (24) ◽  
pp. 12169-12181 ◽  
Author(s):  
Sarah A. Kopecky ◽  
Mark C. Willingham ◽  
Douglas S. Lyles
Keyword(s):  
Gene Expression ◽  
Caspase 3 ◽  
Host Gene ◽  
M Protein ◽  
Host Gene Expression ◽  
Bhk Cells ◽  
Viral Component ◽  
Induction Of Apoptosis ◽  
Induced Apoptosis ◽  
Viral Components

ABSTRACT The induction of apoptosis in host cells is a prominent cytopathic effect of vesicular stomatitis virus (VSV) infection. The viral matrix (M) protein is responsible for several important cytopathic effects, including the inhibition of host gene expression and the induction of cell rounding in VSV-infected cells. This raises the question of whether M protein is also involved in the induction of apoptosis. HeLa or BHK cells were transfected with M mRNA to determine whether M protein induces apoptosis when expressed in the absence of other viral components. Expression of M protein induced apoptotic morphological changes and activated caspase-3 in both cell types, indicating that M protein induces apoptosis in the absence of other viral components. An M protein containing a point mutation that renders it defective in the inhibition of host gene expression (M51R mutation) activated little, if any, caspase-3, while a deletion mutant lacking amino acids 4 to 21 that is defective in the virus assembly function but fully functional in the inhibition of host gene expression was as effective as wild-type (wt) M protein in activating caspase-3. To determine whether M protein influences the induction of apoptosis in the context of a virus infection, the M51R M protein mutation was incorporated onto a wt background by using a recombinant infectious cDNA clone (rM51R-M virus). The timing of the induction of apoptosis by rM51R-M virus was compared to that by the corresponding recombinant wt (rwt) virus and to that by tsO82 virus, the mutant virus in which the M51R mutation was originally identified. In HeLa cells, rwt virus induced apoptosis faster than did rM51R-M virus, demonstrating a role for M protein in the induction of apoptosis. In contrast to the results obtained with HeLa cells, rwt virus induced apoptosis more slowly than did rM51R-M virus in BHK cells. This indicates that a viral component other than M protein contributes to induction of apoptosis in BHK cells and that wt M protein acts to delay induction of apoptosis by the other viral component. tsO82 virus induced apoptosis more rapidly than did rM51R-M virus in both HeLa and BHK cells. These two viruses contain the same point mutation in their M proteins, suggesting that sequence differences in genes other than that for M protein affect their rates of induction of apoptosis.

Suppression of relaxin gene expression by retinoids in squamous differentiated rabbit tracheal epithelial cells

1998 ◽  
Vol 138 (1-2) ◽  
pp. 115-125 ◽  
Author(s):  
Susan H Bernacki ◽  
Alexander Medvedev ◽  
Ginger Holloway ◽  
Marcia Dawson ◽  
Reuben Lotan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

Differential protective effects of Bcl-xL and Bcl-2 on apoptotic liver injury in transgenic mice

1999 ◽  
Vol 277 (3) ◽  
pp. G702-G708 ◽  
Author(s):  
Alix de la Coste ◽  
Monique Fabre ◽  
Nathalie McDonell ◽  
Arlette Porteu ◽  
Helène Gilgenkrantz ◽  
...  
Keyword(s):  
Liver Injury ◽  
Transgenic Mice ◽  
Fas Ligand ◽  
Dependent Manner ◽  
Protective Effects ◽  
Tnf Α ◽  
Apoptotic Pathways ◽  
Induced Apoptosis ◽  
Factor Α

Fas ligand (CD95L) and tumor necrosis factor-α (TNF-α) are pivotal inducers of hepatocyte apoptosis. Uncontrolled activation of these two systems is involved in several forms of liver injury. Although the broad antiapoptotic action of Bcl-2 and Bcl-xL has been clearly established in various apoptotic pathways, their ability to inhibit the Fas/CD95- and TNF-α-mediated apoptotic signal has remained controversial. We have demonstrated that the expression of BCL-2 in hepatocytes protects them against Fas-induced fulminant hepatitis in transgenic mice. The present study shows that transgenic mice overexpressing[Formula: see text]in hepatocytes are also protected from Fas-induced apoptosis in a dose-dependent manner. Bcl-xL and Bcl-2 were protective without any change in the level of endogenous[Formula: see text]or Bax and inhibited hepatic caspase-3-like activity. In vivo injection of TNF-α caused massive apoptosis and death only when transcription was inhibited. Under these conditions,[Formula: see text]mice were partially protected from liver injury and death but PK-BCL-2 mice were not. A similar differential protective effect of Bcl-xL and Bcl-2 transgenes was observed when Fas/CD95 was activated and transcription blocked. These results suggest that apoptosis triggered by activation of both Fas/CD95 and TNF-α receptors is to some extent counteracted by the transcription-dependent protective effects, which are essential for the antiapoptotic activity of Bcl-2 but not of Bcl-xL. Therefore, Bcl-xL and Bcl-2 appear to have different antiapoptotic effects in the liver whose characterization could facilitate their use to prevent the uncontrolled apoptosis of hepatocytes.

scholarly journals Protective Effects of Pretreatment with Quercetin Against Lipopolysaccharide-Induced Apoptosis and the Inhibition of Osteoblast Differentiation via the MAPK and Wnt/β-Catenin Pathways in MC3T3-E1 Cells

2017 ◽  
Vol 43 (4) ◽  
pp. 1547-1561 ◽  
Author(s):  
Chun Guo ◽  
Rui-Juan Yang ◽  
Ke Jang ◽  
Xiao-ling Zhou ◽  
Yu-zhen Liu
Keyword(s):  
Cytochrome C ◽  
Osteoblast Differentiation ◽  
Caspase 3 ◽  
Quantitative Polymerase Chain Reaction ◽  
Bone Diseases ◽  
Cell Counting ◽  
Dependent Manner ◽  
Protective Effects ◽  
Expression Levels ◽  
Induced Apoptosis

Background/Aims: Quercetin, a flavonoid found in onions and other vegetables, has potential inhibitory effects on bone resorption in vivo and in vitro. In our previous study, we found that quercetin treatment reversed lipopolysaccharide (LPS)-induced inhibition of osteoblast differentiation through the mitogen-activated protein kinase (MAPK) pathway in MC3T3-E1 cells. In this study, we investigated the underlying mechanisms of pretreatment with quercetin on apoptosis and the inhibition of osteoblast differentiation in MC3T3-E1 cells induced by LPS. Methods: MC3T3-E1 osteoblasts were treated with quercetin for 2 h; cells were then incubated with LPS in the presence of quercetin for the indicated times. Cell viability was measured using the Cell Counting Kit-8 (CCK-8) assay, and cell apoptosis was evaluated using Hoechst 33258 staining. The mRNA expression levels of osteoblast-specific genes, Bax and caspase-3 were determined by real-time quantitative polymerase chain reaction (qPCR). Protein levels of osteoblast-specific genes, caspase-3, Bax, cytochrome c, Bcl-2, Bcl-XL, phosphorylated MAPKs and Wnt/β-catenin were measured using Western blot assays. The MAPK and Wnt/β-catenin signalling pathways were blocked prior to pretreatment with quercetin. Results: Pretreatment with quercetin significantly restored LPS-suppressed bone mineralization and the mRNA and protein expression levels of osteoblast-specific genes such as Osterix (OSX), runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP) and osteocalcin (OCN) in a dose-dependent manner. Pretreatment with quercetin also inhibited osteoblast apoptosis, significantly restored the down-regulated expression of Bcl-2 and Bcl-XL and decreased the upregulated expression of caspase-3, Bax, and cytochrome c in MC3T3-E1 cells induced by LPS. Furthermore, pretreatment with quercetin not only decreased the abundance of phosphorylated p38 MAPK and increased the abundance of phosphorylated extracellular signal regulated kinase (ERK), but also triggered the Wnt/β-catenin pathway through enhancing expression of Wnt3 and β-catenin. Pretreatment with MAPK inhibitors or the Wnt/β-catenin inhibitor XAV939 blocked the protective effects of quercetin against LPS-induced apoptosis and the inhibition of osteoblast differentiation. Conclusions: Our findings suggest that pretreatment with quercetin may be a potential drug for preventing abnormal human bone loss induced by LPS in bacteria-induced bone diseases.

scholarly journals Icariin Prevents H2O2-Induced Apoptosis via the PI3K/Akt Pathway in Rat Nucleus Pulposus Intervertebral Disc Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiangyu Deng ◽  
Sheng Chen ◽  
Dong Zheng ◽  
Zengwu Shao ◽  
Hang Liang ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Nucleus Pulposus ◽  
Caspase 3 ◽  
Chinese Herb ◽  
Akt Pathway ◽  
Control Group ◽  
Protective Effects ◽  
Nucleus Pulposus Cells ◽  
Intracellular Ros ◽  
Induced Apoptosis

Icariin is a prenylated flavonol glycoside derived from the Chinese herb Epimedium sagittatum. This study investigated the mechanism by which icariin prevents H2O2-induced apoptosis in rat nucleus pulposus (NP) cells. NP cells were isolated from the rat intervertebral disc and they were divided into five groups after 3 passages: (A) blank control; (B) 200 μM H2O2; (C) 200 μM H2O2 + 20 μM icariin; (D) 20 μM icariin + 200 μM H2O2 + 25 μM LY294002; (E) 200 μM H2O2 + 25 μM LY294002. LY294002 is a selective inhibitor of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. NP cell viability, apoptosis rate, intracellular reactive oxygen species levels, and the expression of AKT, p-AKT, p53, Bcl-2, Bax, caspase-3 were estimated. The results show that, compared with the control group, H2O2 significantly increased NP cell apoptosis and the level of intracellular ROS. Icariin pretreatment significantly decreased H2O2-induced apoptosis and intracellular ROS and upregulated p-Akt and BCL-2 and downregulated caspase-3 and Bax. LY294002 abolished the protective effects of icariin. Our results show that icariin can attenuate H2O2-induced apoptosis in rat nucleus pulposus cells and PI3K/AKT pathway is at least partly included in this protection effect.

Sign in / Sign up

Export Citation Format

Share Document