Song, YuRi;Kim, SeYeon;Park, Mee Hee;Na, Hee Sam;Chung, Jin
International Journal of Oral Biology
/
v.42
no.1
/
pp.17-23
/
2017
Background: Periodontitis is generally a chronic disorder characterized by the breakdown of tooth-supporting tissues. P. gingivalis, a Gram-negative anaerobic rod, is one of the major pathogens associated with periodontitis. Frequently, P. gingivalis infection leads to cell death. However, the correlation between P. gingivalis-induced cell death and periodontal inflammation remains to be elucidated. Among cell deaths, the death of immune cells appears to play a significant role in inflammatory response. Thus, the aim of this study was to examine P. gingivalis-induced cell death, focusing on autophagy and apoptosis in THP-1 cells. Methods: Human acute monocytic leukemia cell line (THP-1) was used for all experiments. Autophagy induced by P. gingivalis in THP-1 cells was examined by Cyto ID staining. Intracellular autophagic vacuoles were observed by fluorescence microscopy using staining Acridine orange (AO); and 3-methyladenine (3-MA) was used to inhibit autophagy. Total cell death was measured by LDH assay. Cytokine production was measured by an ELISA method. Results: P. gingivalis induced autophagy in an MOI-dependent manner in THP-1 cells, but 3-MA treatment decreased autophagy and increased the apoptotic blebs. P. gingivalis infection did not increase apoptosis compared to the control cells, whereas inhibition of autophagy by 3-MA significantly increased apoptosis in P. gingivalis-infected THP-1 cells. Inhibition of autophagy by 3-MA also increased total cell deaths and inflammatory cytokine production, including $IL-1{\beta}$ and $TNF-{\alpha}$. Conclusion: P. gingivalis induced autophagy in THP-1 cells, but the inhibition of autophagy by 3-MA stimulated apoptosis, leading to increased cell deaths and pro-inflammatory cytokines production. Hence, the modulation of cell deaths may provide a mechanism to fight against invading microorganisms in host cells and could be a promising way to control inflammation.
Journal of Physiology & Pathology in Korean Medicine
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v.23
no.6
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pp.1409-1415
/
2009
Obesity is especially a serious health problem in industrialized countries, because it is considered to be a risk factor associated with the genesis or development of various metabolic diseases, including cardiovascular disease and type 2 diabetes mellitus. The purpose of this study was to investigate the effects of tanshinone IIA from Salvia miltiorrhiza Bunge on induction of apoptossis and inhibition of adipogenesis in in 3T3-L1 preadipocytes and adipocytes. The results demonstrated that tanshinone IIA decreased cell population growth of 3T3-L1 preadipocytes, assessed with the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] and LDH (lactate dehydrogenase) assay. Flow cytometric analysis of 3T3-L1 preadipocytes exposed to tanshinone IIA showed that apoptotic cells increased in a timeand dose-dependent manner. Treatment with tanshinone IIA decreased the number of normal cells and increased the number of apoptotic cells in a dose-dependent manner. The induction of apoptosis in 3T3-L1 preadipocytes by tanshinone IIA was mediated through the activation of caspase-3 and Bax, and then through the cleavage of PARP and the down-regulation of Bcl-2. Moreover, tanshinone IIA significantly decreased the amount of intracellular triglycerides and GPDH (glycerol-3-phosphate dehydrogenase) activity in 3T3-L1 adipocytes. Our results suggest that tanshinone IIA efficiently induces apoptosis and inhibits adipogenesis in 3T3-L1 preadipocytes and adipocytes.
Kim, Sun-Young;Jeong, Seung-Il;Kim, Sung-Zoo;Shim, Jae-Suk;Jang, Seon-Il
Journal of Physiology & Pathology in Korean Medicine
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v.23
no.6
/
pp.1314-1319
/
2009
In previous study, we have shown that continentalic acid (CA) isolated from Aralia continentalis induced the growth inhibition and apoptosis in HepG2 cells. In this study, we examine the effects of CA from A. continentalis on growth inhibition and apoptosis induction in human leukemia HL-60 and mouse fibroblast NIH 3T3 cell lines. The results demonstrated that CA decreased cell growth of leukemia HL-60 cells but not human HaCaT keratinocytes, assessed with the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] and LDH (lactate dehydrogenase) assay. Flow cytometric analysis of mouse fibroblast cell lines exposed to CA showed that apoptotic cells increased in a time- and dose-dependent manner. Treatment with CA decreased the number of normal cells and increased the number of early apoptotic and late apoptotic cells in a dose-dependent manner. The induction of apoptosis in mouse cell lines by CA was mediated through the activation of caspase-3, Bak, and Bax and the down-regulation of Bcl-2. Our results suggest that CA efficiently induces apoptosis in human leukemia cells.
In recent decades, titanium dioxide ($TiO_2$) nanoparticles have been used in various applications, including paints, coatings, and food. However, data are lacking on the toxicological aspects associated with their use. The aim of this study was to assess the inhalation toxicity of $TiO_2$ nanoparticles in rats by using inhalation exposure. Male Wistar rats were exposed to $TiO_2$ nanoparticles for 2 weeks (6 hr/day, 5 days/week) at a mean mass concentration of $11.39{\pm}0.31mg/m^3$. We performed time-course necropsies at 1, 7, and 15 days after exposure. Lung inflammation and injury were assessed on the basis of the total and individual cell counts in bronchoalveolar lavage fluid (BALF), and by biochemical assays, including an assay for lactate dehydrogenase (LDH). Furthermore, histopathological examination was performed to investigate the lungs and nasal cavity of rats. There were no statistically significant changes in the number of BALF cells, results of biochemical assays of BALF and serum, and results of cytokine analysis. However, we did observe histopathological changes in the nasal cavity tissue. Lesions were observed at post-exposure days 1 and 7, which resolved at post-exposure day 15. We also calculated the actual amounts of $TiO_2$ nanoparticles inhaled by the rats. The results showed that the degree of toxicity induced by $TiO_2$ nanoparticles correlated with the delivered quantities. In particular, exposure to small particles with a size of approximately 20 nm resulted in toxicity, even if the total particle number was relatively low.
Sevoflurane postconditioning (SPostC) has been proved effective in cardioprotection against myocardial ischemia/reperfusion injury. It was also reported that heat shock protein 70 (HSP70) could be induced by sevoflurane, which played a crucial role in hypoxic/reoxygenation (HR) injury of cardiomyocytes. However, the mechanism by which sevoflurane protects cardiomyocytes via HSP70 is still not understood. Here, we aimed to investigate the related mechanisms of SPostC inducing HSP70 expression to reduce the HR injury of cardiomyocytes. After the HR cardiomyocytes model was established, the cells transfected with siRNA for HSP70 (siHSP70) or not were treated with sevoflurane during reoxygenation. The lactate dehydrogenase (LDH) level was detected by colorimetry while cell viability and apoptosis were detected by MTT and flow cytometry. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect HSP70, apoptosis-, cell cycle-associated factors, iNOS, and Cox-2 expressions. Enzyme-linked immuno sorbent assay (ELISA) was used to measure malondialdehyde (MDA) and superoxide dismutase (SOD). SPostC decreased apoptosis, cell injury, oxidative stress and inflammation and increased viability of HR-induced cardiomyocytes. In addition, SPostC downregulated Bax and cleaved caspase-3 levels, while SPostC upregulated Bcl-2, CDK-4, Cyclin D1, and HSP70 levels. SiHSP70 had the opposite effect that SPostC had on HR-induced cardiomyocytes. Moreover, siHSP70 further reversed the effect of SPostC on apoptosis, cell injury, oxidative stress, inflammation, viability and the expressions of HSP70, apoptosis-, and cell cycle-associated factors in HR-induced cardiomyocytes. In conclusion, this study demonstrates that SPostC can reduce the HR injury of cardiomyocytes by inducing HSP70 expression.
Objectives : This study was carried out to evaluate whether the water extract from cause the cellular damage in HepG2 cell line. It was reported that Dictamnus dasycarpus Turcz(DDT) intake induce poisoning symptoms in human population. These symptoms was closely related to liver toxicity, however, mechanisms for liver toxicity caused by DDT have not been elucidated exactly. Here, hepatotoxicity caused by DDT was evaluated using HepG2 cell line. Methods : Water extract of DDT was treated into HepG2 cell with various doses such as 0, 0.1, 0.5, 1.0 and $5.0mg/m{\ell}$. In order to cell viability, both MTT and LDH assay were carried out. Also, apoptosis array kit was used to identify whether cell death caused by DDT is due to apoptosis or not. In addition, reactive oxygen species (ROS) was measured after treatment of water extract. Results : We found out significant changes in the apoptosis related factors of hepatocyte. The cell viability of HepG2 treated with DDT water extract was decreased in dose-dependent. Also most of the apoptosis related factors were significantly increased. We found out that Caspase 3, Cytochrome C and ROS had increased in dose-dependent. In addition, other apoptosis related factors Bcl 2 and Bax, which were also constant changes. However, there was no significance. Conclusions : These results suggest that water soluble extract of DDT is expected to have oral toxicity, including hepatocellular damage Therefore, it is suggested that DDT could cause various side effects and toxicity of clinical conditions.
Background: Korean Red Ginseng (KRG) was reported to play an anti-inflammatory role, however, previous studies largely focused on the effects of KRG on priming step, the inflammation-preparing step, and the anti-inflammatory effect of KRG on triggering, the inflammation-activating step has been poorly understood. This study demonstrated anti-inflammatory role of KRG in caspase-11 non-canonical inflammasome activation in macrophages during triggering of inflammatory responses. Methods: Caspase-11 non-canonical inflammasome-activated J774A.1 macrophages were established by priming with Pam3CSK4 and triggering with lipopolysaccharide (LPS). Cell viability and pyroptosis were examined by MTT and lactate dehydrogenase (LDH) assays. Nitric oxide (NO)-inhibitory effect of KRG was assessed using a NO production assay. Expression and proteolytic cleavage of proteins were examined by Western blotting analysis. In vivo anti-inflammatory action of KRG was evaluated with the LPS-injected sepsis model in mice. Results: KRG reduced LPS-stimulated NO production in J774A.1 cells and suppressed pyroptosis and IL-1β secretion in caspase-11 non-canonical inflammasome-activated J774A.1 cells. Mechanistic studies demonstrated that KRG suppressed the direct interaction between LPS and caspase-11 and inhibited proteolytic processing of both caspase-11 and gasdermin D in caspase-11 non-canonical inflammasome-activated J774A.1 cells. Furthermore, KRG significantly ameliorated LPS-mediated lethal septic shock in mice. Conclusion: The results demonstrate a novel mechanism of KRG-mediated anti-inflammatory action that operates through targeting the caspase-11 non-canonical inflammasome at triggering step of macrophage-mediated inflammatory response.
Xue Yan;Liang Jin;Huifen Zhou;Haofang Wan;Haitong Wan;Jiehong Yang
Journal of Microbiology and Biotechnology
/
v.33
no.10
/
pp.1281-1291
/
2023
Infectious diseases caused by drug-resistant Escherichia coli (E. coli) pose a critical concern for medical institutions as they can lead to high morbidity and mortality rates. In this study, amygdalin exhibited anti-inflammatory and antioxidant activities, as well as other potentials. However, whether it could influence the drug-resistant E. coli-infected cells remained unanswered. Amygdalin was therefore tested in a cellular model in which human macrophages were exposed to resistant E. coli. Apoptosis was measured by flow cytometry and the lactate dehydrogenase (LDH) assay. Western immunoblotting and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to quantify interleukin-18 (IL-18), interleukin-1β (IL-1β), and interleukin-6 (IL-6). The production of reactive oxygen species (ROS) in macrophages was detected by ROS kit. The expression of pan-apoptotic proteins in macrophages was measured by qRT-PCR and Western immunoblotting. Drug-Resistant E. coli inhibited cell viability and enhanced apoptosis in the cellular model. In cells treated with amygdalin, this compound can inhibit cell apoptosis and reduce the expression of pro - inflammatory cytokines such as IL-1β, IL-18 and IL-6. Additionally, it decreases the production of PANoptosis proteins, Furthermore, amygdalin lowered the levels of reactive oxygen species induced by drug-resistant E. coli, in cells, demonstrating its antioxidant effects. Amygdalin, a drug with a protective role, alleviated cell damage caused by drug-resistant E. coli in human macrophages by inhibiting the PANoptosis signaling pathway.
Objectives : In this study, the author tried to investigate whether wood vinegar produced from Morus alba (MA) significantly affects the increase in airway epithelial mucosubstances and hyperplasia of tracheal goblet cells of rats, and in vitro airway mucin secretion and PMA- or EGF- or TNF-alpha-induced MUC5AC mucin production / gene expression from human airway epithelial cells. Materials and Methods : For the in vivo experiment, the author induced hypersecretion of airway mucus and goblet cell hyperplasia by exposure of rats to SO2 over 3 weeks. Effect of orally-administered MA over 2 weeks on increase in airway epithelial mucosubstances from tracheal goblet cells of rats and hyperplasia of goblet cells were assessed using histopathological analysis after staining the epithelial tissue with alcian blue. For the in vitro experiment, confluent RTSE cells were chased for 30 min in the presence of MA to assess the effect of MA on mucin secretion by enzyme-linked immunosorbent assay (ELISA). Also, effects of MA on PMA- or EGF- or TNF-alpha-induced MUC5AC mucin production and gene expression from human airway epithelial cells (NCI-H292) were investigated. Confluent NCI-H292 cells were pretreated for 30 min in the presence of MA and treated with PMA (10 ng/ml), EGF (25 ng/ml) or TNF-alpha (0.2 nm) for 24 hrs, to assess both effects of MA on PMA- or EGF- or TNF-alpha-induced MUC5AC mucin production by enzyme-linked immunosorbent assay (ELISA) and gene expression by reverse transcription-polymerase chain reaction (RT-PCR). Possible cytotoxicities of MA in vitro were assessed by examining LDH release from RTSE cells and the rate of survival and proliferation of NCI-H292 cells. In vivo liver and kidney toxicities of MA were evaluated by measuring serum GOT/GPT activities and serum BUN/creatinine concentrations of rats after administering MA orally. Results : 1. MA decreased the amount of intraepithelial mucosubstances of rats exposed to sulfur dioxide inhalationally. 2. MA decreased in vitro mucin secretion from cultured RTSE cells. 3. MA significantly inhibited PMA-, EGF-, and TNF-alpha-induced MUC5AC mucin productions and the expression levels of MUC5AC mRNA from NCI-H292 cells. 4. MA did not show either in vitro or in vivo hepatic or renal toxicities. Conclusion : The results from this study suggests that MA can regulate the secretion, production and gene expression of airway mucin observed in diverse respiratory diseases accompanied by mucus hypersecretion and does not show in vivo toxicity to liver and kidney functions after oral administration. Effects of MA should be further studied using animal experimental models that simulate the diverse pathophysiology of respiratory diseases via future research.
Chlamydiae, obligate intracellular bacteria, are associated with a variety of human diseases. The chlamydial life cycle undergoes a biphasic development: replicative reticulate bodies (RBs) phase and infectious elementary bodies (EBs) phase. At the end of the chlamydial intracellular life cycle, EBs have to be released to the surrounded cells. Therefore, the interactions between Chlamydiae and cell death pathways could greatly influence the outcomes of Chlamydia infection. However, the underlying molecular mechanisms remain elusive. Here, we investigated host cell death after Chlamydia infection in vitro, in L929 cells, and showed that Chlamydia infection induces cell necrosis, as detected by the propidium iodide (PI)-Annexin V double-staining flow-cytometric assay and Lactate dehydrogenase (LDH) release assay. The production of reactive oxygen species (ROS), an important factor in induction of necrosis, was increased after Chlamydia infection, and inhibition of ROS with specific pharmacological inhibitors, diphenylene iodonium (DPI) or butylated hydroxyanisole (BHA), led to significant suppression of necrosis. Interestingly, live-cell imaging revealed that Chlamydia infection induced lysosome membrane permeabilization (LMP). When an inhibitor upstream of LMP, CA-074-Me, was added to cells, the production of ROS was reduced with concomitant inhibition of necrosis. Taken together, our results indicate that Chlamydia infection elicits the production of ROS, which is dependent on LMP at least partially, followed by induction of host-cell necrosis. To our best knowledge, this is the first live-cell-imaging observation of LMP post Chlamydia infection and report on the link of LMP to ROS to necrosis during Chlamydia infection.
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