scholarly journals Protective Effects of Ethanol Extract of Brazilian Green Propolis and Apigenin against Weak Ultraviolet Ray-B-Induced Barrier Dysfunction via Suppressing Nitric Oxide Production and Mislocalization of Claudin-1 in HaCaT Cells

2021 ◽  
Vol 22 (19) ◽  
pp. 10326
Author(s):  
Yuta Yoshino ◽  
Kana Marunaka ◽  
Mao Kobayashi ◽  
Haruka Matsunaga ◽  
Shokoku Shu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Ethanol Extract ◽  
Hydroxyl Group ◽  
No Production ◽  
Hacat Cells ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Uvb Irradiation ◽  
Ultraviolet Ray ◽  
Brazilian Green Propolis

Once weak ultraviolet ray-B (UVB) irradiates the skin cells, the generation of reactive nitrogen species (RNS), but not reactive oxygen species (ROS), is stimulated for the mislocalization of claudin-1 (CLDN1), an essential protein for forming tight junctions (TJs). Since our skin is constantly exposed to sunlight throughout our lives, an effective protection strategy is needed to maintain the skin barrier against weak UVB. In the present study, we investigated whether an ethanol extract of Brazilian green propolis (EBGP) and flavonoids had a protective effect against weak UVB irradiation-induced barrier dysfunction in human keratinocyte-derived HaCaT cells. A pretreatment with EBGP suppressed TJ permeability, RNS production, and the nitration level of CLDN1 in the weak UVB-exposed cells. Among the propolis components, apigenin and apigenin-like flavonoids have potent protective effects against NO production and the mislocalization of CLDN1 induced by UVB. The analyses between structures and biological function revealed that the chemically and structurally characteristic flavonoids with a hydroxyl group at the 4′ position on the B-ring might contribute to its protective effect on barrier dysfunction caused by weak UVB irradiation. In conclusion, EBGP and its component apigenin protect HaCaT cells from weak UVB irradiation-induced TJ barrier dysfunction mediated by suppressing NO production.

scholarly journals Sargassum fulvellumProtects HaCaT Cells and BALB/c Mice from UVB-Induced Proinflammatory Responses

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Chan Lee ◽  
Gyu Hwan Park ◽  
Eun Mi Ahn ◽  
Chan-Ik Park ◽  
Jung-Hee Jang
Keyword(s):  
Nitric Oxide ◽  
Ethanol Extract ◽  
Prostaglandin E ◽  
Hacat Cells ◽  
Uvb Irradiation ◽  
Proinflammatory Mediators ◽  
Sargassum Fulvellum ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Skin Damages

Ultraviolet (UV) radiation has been reported to induce cutaneous inflammation such as erythema and edema via induction of proinflammatory enzymes and mediators.Sargassum fulvellumis a brown alga of Sargassaceae family which has been demonstrated to exhibit antipyretic, analgesic, antiedema, antioxidant, antitumor, fibrinolytic, and hepatoprotective activities. The purpose of this study is to investigate anti-inflammatory effects of ethylacetate fraction of ethanol extract ofSargassum fulvellum(SFE-EtOAc) in HaCaT keratinocytes and BALB/c mice. In HaCaT cells, SFE-EtOAc effectively inhibited UVB-induced cytotoxicity (60 mJ/cm2) and the expression of proinflammatory proteins such as cyclooxygenase-2 (COX-2), tumor necrosis factor-α(TNF-α), and inducible nitric oxide synthase (iNOS). Furthermore, SFE-EtOAc significantly reduced UVB-induced production of proinflammatory mediators including prostaglandin E2(PGE2) and nitric oxide (NO). In BALB/c mice, topical application of SFE-EtOAc prior to UVB irradiation (200 mJ/cm2) effectively suppressed the UVB-induced protein expression of COX-2, iNOS, and TNF-αand subsequently attenuated generation of PGE2and NO as well. In another experiment, SFE-EtOAc pretreatment suppressed UVB-induced reactive oxygen species production and exhibited an antioxidant potential by upregulation of antioxidant enzymes such as catalase and Cu/Zn-superoxide dismutase in HaCaT cells. These results suggest that SFE-EtOAc could be an effective anti-inflammatory agent protecting against UVB irradiation-induced skin damages.

Anti-Apoptotic and Anti-Inflammatory Activities of Edible Fresh Water Algae Prasiola japonica in UVB-Irradiated Skin Keratinocytes

2019 ◽  
Vol 47 (08) ◽  
pp. 1853-1868
Author(s):  
Eunju Choi ◽  
Young-Su Yi ◽  
Jongsung Lee ◽  
Sang Hee Park ◽  
Sunggyu Kim ◽  
...  
Keyword(s):  
Fresh Water ◽  
Ethanol Extract ◽  
The Body ◽  
Hacat Cells ◽  
Protective Effects ◽  
Proteolytic Activation ◽  
Skin Keratinocytes ◽  
External Stresses ◽  
Anti Oxidant ◽  
Anti Inflammatory

Skin is the outer tissue layer and is a barrier protecting the body from various external stresses. The fresh water green edible algae Prasiola japonica has antiviral, antimicrobial, and anti-inflammatory properties; however, few studies of its effects on skin-protection have been reported. In this study, Prasiola japonica ethanol extract (Pj-EE) was prepared, and its skin-protective properties were investigated in skin keratinocytes. Pj-EE inhibited ROS production in UVB-irradiated HaCaT cells without cytotoxicity. Pj-EE also suppressed the apoptotic death of UVB-irradiated HaCaT cells by decreasing the generation of apoptotic bodies and the proteolytic activation of apoptosis caspase-3, -8, and -9. Moreover, Pj-EE downregulated the mRNA expression of the inflammatory gene cyclooxygenase-2 (COX-2), the pro-inflammatory cytokine genes interleukin (IL)-1[Formula: see text], IL-8, IL-6, tumor necrosis factor (TNF)-[Formula: see text], and interferon (IFN)-[Formula: see text], and the tissue remodeling genes matrix metalloproteinase (MMP)-1, -2, -3, and -9. The Pj-EE-induced anti-inflammatory effect was mediated by suppressing the activation of nuclear factor-kappa B (NF-[Formula: see text]B) signaling pathway in the UVB-irradiated HaCaT cells. Taken together, these results suggest that Pj-EE exerts skin-protective effects through anti-oxidant, anti-apoptotic, and anti-inflammatory activities in skin keratinocytes.

scholarly journals Hypoxia-inducible factor hydroxylase inhibition enhances the protective effects of cyclosporine in colitis

2019 ◽  
Vol 317 (2) ◽  
pp. G90-G97 ◽  
Author(s):  
Doug N. Halligan ◽  
Mohammed N. Khan ◽  
Eric Brown ◽  
Catherine R. Rowan ◽  
Ivan S. Coulter ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Protective Effect ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Function ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Inflammatory bowel disease (IBD) is characterized by epithelial barrier dysfunction with resultant inflammation as the mucosal immune system becomes exposed to luminal antigens. The hydroxylase inhibitor dimethyloxalylglycine (DMOG) reduces symptoms in experimental colitis through the upregulation of genes promoting barrier function and inhibition of epithelial cell apoptosis. The immunosuppressive drug cyclosporine reduces inflammation associated with IBD via suppression of immune cell activation. Given the distinct barrier protective effect of DMOG and the anti-inflammatory properties of cyclosporine, we hypothesized that combining these drugs may provide an enhanced protective effect by targeting both barrier dysfunction and inflammation simultaneously. We used the dextran sulfate sodium model of colitis in C57BL/6 mice to determine the combinatorial efficacy of cyclosporine and DMOG. While cyclosporine and DMOG ameliorated disease progression, in combination they had an additive protective effect that surpassed the level of protection afforded by either drug alone. The ability of DMOG to augment the anti-inflammatory effects of cyclosporine was largely due to preservation of barrier function and at least in part due to zonula occludens-1 regulation. We propose that combining the barrier protective effects of a hydroxylase inhibitor with the anti-inflammatory effects of cyclosporine provides added therapeutic benefit in colitis. NEW & NOTEWORTHY Inflammatory bowel disease is the result of decreased intestinal epithelial barrier function leading to exposure of the mucosal immune system to luminal antigens causing inflammation, which in turn further decreases epithelial barrier function. We demonstrate for the first time that strengthening the epithelial barrier with a hydroxylase inhibitor in combination with the administration of the immunosuppressive cyclosporine provides additive therapeutic advantage in a murine model of colitis

scholarly journals Protective Effect of Antrodia cinnamomea Extract against Irradiation-Induced Acute Hepatitis

2019 ◽  
Vol 20 (4) ◽  
pp. 846 ◽  
Author(s):  
Tsu-Hsiang Kuo ◽  
Yueh-Hsiung Kuo ◽  
Chun-Yu Cho ◽  
Chih-Jung Yao ◽  
Gi-Ming Lai ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Protective Effect ◽  
Acute Hepatitis ◽  
Ethanol Extract ◽  
Normal Liver ◽  
Protective Effects ◽  
Active Components ◽  
Normal Liver Cell ◽  
Antrodia Cinnamomea ◽  
Tumor Bearing

Radiotherapy for treatment of hepatocellular carcinoma causes severe side effects, including acute hepatitis and chronic fibrosis. Complementary and alternative medicine (CAM) has emerged as an important part of integrative medicine in the management of diseases. Antrodia cinnamomea (AC), a valuable medicinal fungus originally found only in Taiwan, has been shown to possess anti-oxidation, vaso-relaxtation, anti-inflammation, anti-hepatitis, and anti-cancer effects. In this paper we evaluate the protective effects of ethanol extract of Antrodia cinnamomea (ACE) against radiotoxicity both in normal liver cell line CL48 and in tumor-bearing mice. In CL48, ACE protects cells by eliminating irradiation-induced reactive oxygen species (ROS) through the induction of Nrf2 and the downstream redox system enzymes. The protective effect of ACE was also demonstrated in tumor-bearing mice by alleviating irradiation-induced acute hepatitis. ACE could also protect mice from CCl4-induced hepatitis. Since both radiation and CCl4 cause free radicals, these results indicate that ACE likely contains active components that protect normal liver cells from free radical attack and can potentially benefit hepatocellular carcinoma (HCC) patients during radiotherapy.

scholarly journals Carbon Monoxide Protects against Liver Failure through Nitric Oxide–induced Heme Oxygenase 1

2003 ◽  
Vol 198 (11) ◽  
pp. 1707-1716 ◽  
Author(s):  
Brian S. Zuckerbraun ◽  
Timothy R. Billiar ◽  
Sherrie L. Otterbein ◽  
Peter K.M. Kim ◽  
Fang Liu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Cell Death ◽  
Protective Effect ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
No Production ◽  
Protective Effects ◽  
In Vivo Models

Carbon monoxide (CO) and nitric oxide (NO) each have mechanistically unique roles in various inflammatory disorders. Although it is known that CO can induce production of NO and that NO can induce expression of the cytoprotective enzyme heme oxygenase 1 (HO-1), there is no information whether the protective effect of CO ever requires NO production or whether either gas must induce expression of HO-1 to exert its functional effects. Using in vitro and in vivo models of tumor necrosis factor α–induced hepatocyte cell death in mice, we find that activation of nuclear factor κB and increased expression of inducible NO are required for the protective effects of CO, whereas the protective effects of NO require up-regulation of HO-1 expression. When protection from cell death is initiated by CO, NO production and HO-1 activity are each required for the protective effect showing for the first time an essential synergy between these two molecules in tandem providing potent cytoprotection.

scholarly journals Oat (Avena sativa) Extract against Oxidative Stress-Induced Apoptosis in Human Keratinocytes

Molecules ◽  
2021 ◽  
Vol 26 (18) ◽  
pp. 5564
Author(s):  
Sooji Song ◽  
Yoon-Mi Lee ◽  
Yu Young Lee ◽  
Kyung-Jin Yeum
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cell Death ◽  
Protective Effect ◽  
Avena Sativa ◽  
Ethanol Extract ◽  
Human Keratinocytes ◽  
Hacat Cells ◽  
Ethanol Extracts ◽  
Induced Apoptosis

Oat (Avena sativa) is well known for its various health benefits. The protective effect of oat extract against oxidative stress-induced apoptosis in human keratinocytes HaCaT was determined. First, extracts of two varieties of oat, Daeyang and Choyang, were analyzed for fat-soluble antioxidants such as α-tocotrienol, γ-oryzanols, lutein and zeaxanthin using an UPLC system and for antioxidant activity using a DPPH assay. Specifically, an 80% ethanol extract of Daeyang oat (Avena sativa cv. Daeyang), which had high amounts of antioxidants and potent radical scavenging activity, was further evaluated for protective effect against oxidative stress-induced cell death, intracellular reactive oxygen species levels, the phosphorylation of DNA damage mediating genes such as H2AX, checkpoint kinase 1 and 2, and p53 and the activation of apoptotic genes such as cleaved caspase-3 and 7 and poly (ADP-ribose) polymerase in HaCaT cells. The Daeyang and Choyang oat 80% ethanol extracts had 26.9 and 24.1 mg/100 g γ-oryzanols, 7.69 and 8.38 mg/100 g α-tocotrienol, 1.25 and 0.34 mg/100 g of lutein and 1.20 and 0.17 mg/100 g of zeaxanthin, respectively. The oat 80% ethanol extract treatment (Avena sativa cv. Daeyang) had a protective effect on oxidative stress-induced cell death in HaCaT cells. In addition, the oat 80% ethanol extracts led to a significant decrease in the intracellular ROS level at a concentration of 50–200 μg/mL, the attenuation of DNA damage mediating genes and the inhibition of apoptotic caspase activities in a dose dependent manner (50–200 μg/mL). Thus, the current study indicates that an oat (Avena sativa cv. Daeyang) extract rich in antioxidants, such as polyphenols, avenanthramides, γ-oryzanols, tocotrienols and carotenoids, has a protective role against oxidative stress-induced keratinocyte injuries and that oat may a useful source for oxidative stress-associated skin damage.

Protective effects of intravascular pressure and nitric oxide in ischemic lung injury

1998 ◽  
Vol 84 (3) ◽  
pp. 803-808 ◽  
Author(s):  
Patrice M. Becker ◽  
Wendy Buchanan ◽  
J. T. Sylvester
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Lung Injury ◽  
Physiological Salt Solution ◽  
No Production ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Shear Forces ◽  
Osmotic Reflection Coefficient ◽  
Intravascular Pressure

Cessation of blood flow during ischemia will decrease both distending and shear forces exerted on endothelium and may worsen ischemic lung injury by decreasing production of nitric oxide (NO), which influences vascular barrier function. We hypothesized that increased intravascular pressure (Piv) during ventilated ischemia might maintain NO production by increasing endothelial stretch or shear forces, thereby attenuating ischemic lung injury. Injury was assessed by measuring the filtration coefficient ( Kf) and the osmotic reflection coefficient for albumin (ςalb) after 3 h of ventilated (95% O2-5% CO2; expiratory pressure 3 mmHg) ischemia. Lungs were flushed with physiological salt solution, and then Piv was adjusted to achieve High Piv (mean 6.7 ± 0.4 mmHg, n = 15) or Low Piv (mean 0.83 ± 0.4 mmHg, n = 10). NG-nitro-l-arginine methyl ester (l-NAME; 10−5M, n = 10), NG-nitro-d-arginine methyl ester (d-NAME; 10−5M, n = 11), orl-NAME (10−5M)+l-arginine (5 × 10−4M, n = 6) was added at the start of ischemia in three additional groups of lungs with High Piv. High Piv attenuated ischemic injury compared with Low Piv (ςalb0.67 ± 0.04 vs. 0.35 ± 0.04, P < 0.05). The protective effect of High Piv was abolished byl-NAME (ςalb0.37 ± 0.04, P < 0.05) but not byd-NAME (ςalb0.63 ± 0.07). The effects of l-NAME were overcome by an excess of l-arginine (ςalb0.56 ± 0.05, P < 0.05). Kfdid not differ significantly among groups. These results suggest that Piv modulates ischemia-induced barrier dysfunction in the lung, and these effects may be mediated by NO.

scholarly journals Brazilian Green Propolis Rescues Oxidative Stress-Induced Mislocalization of Claudin-1 in Human Keratinocyte-Derived HaCaT Cells

2019 ◽  
Vol 20 (16) ◽  
pp. 3869 ◽  
Author(s):  
Kana Marunaka ◽  
Mao Kobayashi ◽  
Shokoku Shu ◽  
Toshiyuki Matsunaga ◽  
Akira Ikari
Keyword(s):  
Oxidative Stress ◽  
Lucifer Yellow ◽  
Ethanol Extract ◽  
Paracellular Permeability ◽  
Hacat Cells ◽  
Fluorescent Marker ◽  
Human Keratinocyte ◽  
Phosphatase 2A ◽  
And Oxidative Stress ◽  
Brazilian Green Propolis

Claudin-1 (CLDN1) is expressed in the tight junction (TJ) of the skin granular layer and acts as a physiological barrier for the paracellular transport of ions and nonionic molecules. Ultraviolet (UV) and oxidative stress may disrupt the TJ barrier, but the mechanism of and protective agents against this effect have not been clarified. We found that UVB and hydrogen peroxide (H2O2) caused the internalization of CLDN1 and increased the paracellular permeability of lucifer yellow, a fluorescent marker, in human keratinocyte-derived HaCaT cells. Therefore, the mechanism of mislocalization of CLDN1 and the protective effect of an ethanol extract of Brazilian green propolis (EBGP) were investigated. The UVB- and H2O2-induced decreases in CLDN1 localization were rescued by EBGP. H2O2 decreased the phosphorylation level of CLDN1, which was also rescued by EBGP. Wild-type CLDN1 was distributed in the cytosol after treatment with H2O2, whereas T191E, its H2O2-insensitive phosphorylation-mimicking mutant, was localized at the TJ. Both protein kinase C activator and protein phosphatase 2A inhibitor rescued the H2O2-induced decrease in CLDN1 localization. The tight junctional localization of CLDN1 and paracellular permeability showed a negative correlation. Our results indicate that UVB and H2O2 could induce the elevation of paracellular permeability mediated by the dephosphorylation and mislocalization of CLDN1 in HaCaT cells, which was rescued by EBGP. EBGP and its components may be useful in preventing the destruction of the TJ barrier through UV and oxidative stress.

Sign in / Sign up

Export Citation Format

Share Document