scholarly journals Tryptophan Photoproduct FICZ Upregulates IL1A, IL1B, and IL6 Expression via Oxidative Stress in Keratinocytes

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yuka Tanaka ◽  
Hiroshi Uchi ◽  
Akiko Hashimoto-Hachiya ◽  
Masutaka Furue
Keyword(s):  
Proinflammatory Cytokine ◽  
Protein Product ◽  
Ultraviolet B ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Hacat Keratinocytes ◽  
Uvb Irradiation ◽  
Aryl Hydrocarbon ◽  
Uvb Exposure

Ultraviolet B (UVB) irradiation activates the aryl hydrocarbon receptor (AHR), generates the reactive oxygen species (ROS), and induces the production of proinflammatory cytokines such as IL1A, IL1B, and IL6. 6-Formylindolo[3,2-b]carbazole (FICZ) is a tryptophan-derived photoproduct that is induced by UVB irradiation and activates the AHR. However, its role in upregulating proinflammatory cytokine expression has never been investigated. Here, we demonstrated that FICZ enhanced ROS generation in human HaCaT keratinocytes in an AHR-dependent manner. FICZ also upregulated the expression of IL1A and IL1B, as well as the expression of IL6 and the production of its protein product, in an AHR- and ROS-dependent fashion. Here, we demonstrate that the actions of FICZ can substitute for the hazardous effects of UVB exposure, contributing to the further understandings of the mechanisms which UVB harms organisms.

scholarly journals Echinacoside Alleviates UVB Irradiation-Mediated Skin Damage via Inhibition of Oxidative Stress, DNA Damage, and Apoptosis

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Di Zhang ◽  
Chengtao Lu ◽  
Zhe Yu ◽  
Xiayin Wang ◽  
Li Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Histopathological Examination ◽  
Ultraviolet B ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Skin Damage ◽  
Uvb Irradiation ◽  
Uvb Exposure

Ultraviolet B (UVB) irradiation has been known to cause skin damage, which is associated with oxidative stress, DNA damage, and apoptosis. Echinacoside is a phenylethanoid glycoside isolated from Herba Cistanches, which exhibits strong antioxidant activity. In this study, we evaluate the photoprotective effect of echinacoside on UVB-induced skin damage and explore the potential molecular mechanism. BALB/c mice and HaCaT cells were treated with echinacoside before UVB exposure. Histopathological examination was used to evaluate the skin damage. Cell viability, lactate dehydrogenase (LDH) levels, antioxidant enzyme activities, reactive oxygen species (ROS) generation, DNA damage, and apoptosis were measured as well. Western blot was used to measure the expression of related proteins. The results revealed that pretreatment of echinacoside ameliorated the skin injury; attenuated oxidative stress, DNA damage, and apoptosis caused by UVB exposure; and normalized the protein levels of ATR, p53, PIAS3, hnRNP K, PARP, and XPA. To summarize, echinacoside is beneficial in the prevention of UVB-induced DNA damage and apoptosis of the skin in vivo and in vitro.

scholarly journals Ethyl Rosmarinate Protects High Glucose-Induced Injury in Human Endothelial Cells

Molecules ◽  
2018 ◽  
Vol 23 (12) ◽  
pp. 3372 ◽  
Author(s):  
Yan-Hui Shen ◽  
Li-Ying Wang ◽  
Bao-Bao Zhang ◽  
Qi-Ming Hu ◽  
Pu Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Protective Effect ◽  
High Glucose ◽  
Reactive Oxygen ◽  
Annexin V ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Jnk Pathway

Ethyl rosmarinate (RAE) is one of the active constituents from Clinopodium chinense (Benth.) O. Kuntze, which is used for diabetic treatment in Chinese folk medicine. In this study, we investigated the protective effect of RAE on high glucose-induced injury in endothelial cells and explored its underlying mechanisms. Our results showed that both RAE and rosmarinic acid (RA) increased cell viability, decreased the production of reactive oxygen species (ROS), and attenuated high glucose-induced endothelial cells apoptosis in a dose-dependent manner, as evidenced by Hochest staining, Annexin V–FITC/PI double staining, and caspase-3 activity. RAE and RA both elevated Bcl-2 expression and reduced Bax expression, according to Western blot. We also found that LY294002 (phosphatidylinositol 3-kinase, or PI3K inhibitor) weakened the protective effect of RAE. In addition, PDTC (nuclear factor-κB, or NF-κB inhibitor) and SP600125 (c-Jun N-terminal kinase, or JNK inhibitor) could inhibit the apoptosis in endothelial cells caused by high glucose. Further, we demonstrated that RAE activated Akt, and the molecular docking analysis predicted that RAE showed more affinity with Akt than RA. Moreover, we found that RAE inhibited the activation of NF-κB and JNK. These results suggested that RAE protected endothelial cells from high glucose-induced apoptosis by alleviating reactive oxygen species (ROS) generation, and regulating the PI3K/Akt/Bcl-2 pathway, the NF-κB pathway, and the JNK pathway. In general, RAE showed greater potency than RA equivalent.

scholarly journals Acetylshikonin Induces Apoptosis in Human Colorectal Cancer HCT-15 and LoVo Cells via Nuclear Translocation of FOXO3 and ROS Level Elevation

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Heui Min Lim ◽  
Jongsung Lee ◽  
Myeong Jin Nam ◽  
See-Hyoung Park
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Nuclear Translocation ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Human Colorectal Cancer ◽  
Antiproliferative Effects ◽  
Lovo Cells ◽  
Colorectal Cancer Cells

Acetylshikonin, a naphthoquinone, is a pigment compound derived from Arnebia sp., which is known for its anti-inflammatory potential. However, its anticarcinogenic effect has not been well investigated. Thus, in this study, we focused on investigating its apoptotic effects against HCT-15 and LoVo cells, which are human colorectal cancer cells. MTT assay, cell counting assay, and colony formation assay have shown acetylshikonin treatment induced cytotoxic and antiproliferative effects against colorectal cancer cells in a dose- and time-dependent manner. DNA fragmentation was observed via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Also, the increase of subG1 phase in cell cycle arrest assay and early/late apoptotic rates in annexin V/propidium iodide (PI) double staining assay was observed, which indicates an apoptotic potential of acetylshikonin against colorectal cancer cells. 2 ′ ,7 ′ -Dichlorofluorescin diacetate (DCF-DA) staining was used to evaluate reactive oxygen species (ROS) generation in acetylshikonin-treated colorectal cancer cells. Fluorescence-activated cell sorting (FACS) analysis showed that acetylshikonin induced an increase in reactive oxygen species (ROS) levels and apoptotic rate in a dose- and time-dependent manner in HCT-15 and LoVo cells. In contrast, cotreatment with N-acetyl cysteine (NAC) has reduced ROS generation and antiproliferative effects in colorectal cancer cells. Western blotting analysis showed that acetylshikonin treatment induced increase of cleaved PARP, γH2AX, FOXO3, Bax, Bim, Bad, p21, p27, and active forms of caspase-3, caspase-7, caspase-9, caspase-6, and caspase-8 protein levels, while those of inactive forms were decreased. Also, the expressions of pAkt, Bcl-2, Bcl-xL, peroxiredoxin, and thioredoxin 1 were decreased. Furthermore, western blotting analysis of cytoplasmic and nuclear fractionated proteins showed that acetylshikonin treatment induced the nuclear translocation of FOXO3, which might result from DNA damage by the increased intracellular ROS level. This study represents apoptotic potential of acetylshikonin against colorectal cancer cells via translocation of FOXO3 to the nucleus and upregulation of ROS generation.

The Requirement of Reactive Oxygen Species Generation in the Apoptosis of Leukemia Cells Induced by 2-Methoxyestradiol.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4370-4370
Author(s):  
Guo Kunyuan ◽  
Miaorong She ◽  
Haiyan Hu ◽  
Xinqing Niu ◽  
Sanfang Tu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Leukemia Cell ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Leukemic Cells ◽  
Leukemia Cells ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Induced Apoptosis

Abstract 2-Methoxyestradiol (2-ME) is a new anticancer agent currently under investigation for treatment of leukemia. We evaluated the effects of 2-ME-induced apoptosis in two myeloid leukemia cell lines (U937 and HL-60) in association with reactive oxygen species (ROS) generation. We found that 2-ME resulted in viability decrease in a dose-dependent manner, generated ROS: nitric oxide and superoxide anions, and mitochondria damage. 2-ME-induced apoptosis correlated with increase in ROS. Quenching of ROS with N-acetyl-L-cysteine protected leukemia cells from the cytotoxicity of 2-ME and prevented apoptosis induction by 2-ME. Furthermore, addition of manumycin, a farnesyltransferase inhibitor, demonstrated by our previous studies that induced apoptosis of leukemic cells and induced ROS, significantly enhanced the apoptosis-induced by 2-ME. In conclusion, cellular ROS generation play an important role in the cytotoxic effect of 2-ME. It is possible to use ROS-generation agents such as manumycin to enhance the antileukemic effect. Such a combination strategy need the further in vivo justify and may have potential clinical application.

scholarly journals ANG II promotes autophagy in podocytes

2010 ◽  
Vol 299 (2) ◽  
pp. C488-C496 ◽  
Author(s):  
Anju Yadav ◽  
Sridevi Vallabu ◽  
Shitij Arora ◽  
Pranay Tandon ◽  
Divya Slahan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Ang Ii ◽  
Electron Microscopic ◽  
Glomerular Filtration Barrier ◽  
Filtration Barrier ◽  
Microscopic Studies ◽  
Autophagic Process

Podocytes are an integral and important constituent of the glomerular filtration barrier (GFB) and are exposed to a higher concentrations of ANG II in diseased states; consequently, podocytes may accumulate oxidized proteins and damaged mitochondria. In the present study, we evaluated the effect of ANG II on the podocyte autophagic process, which is likely to be triggered in order to degrade unwanted proteins and damaged organelles. To quantitate the occurrence of autophagy, electron microscopic studies were carried out on control and ANG II-treated conditionally immortalized mouse podocytes (CIMPs). ANG II-treated cells showed a fivefold greater number of autophagosomes/field compared with control cells. This proautophagic effect of ANG II was inhibited by pretreatment with 3-methyladenine, an inhibitor of autophagy. ANG II also enhanced podocyte expression of autophagic genes such as LC3-2 and beclin-1. Since oxidative stress is often associated with the induction of autophagy, we examined the effect of ANG II on podocyte reactive oxygen species (ROS) generation. ANG II enhanced podocyte ROS generation in a time-dependent manner. To determine whether there is a causal relationship between ANG II-induced oxidative stress and induction of autophagy, we evaluated the effect of antioxidants on ANG II-induced autophagy. As expected, the proautophagic effect of ANG II was inhibited by antioxidants. We conclude that ANG II promotes podocyte autophagy through the generation of ROS.

scholarly journals The acute toxicity of Oxydemeton-methyl in zebrafish

2017 ◽  
Author(s):  
Guofeng Jia ◽  
Xiecheng Liu
Keyword(s):  
Water Solubility ◽  
Harmful Effect ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Male And Female ◽  
P450 Reductase ◽  
Microsomal Cytochrome P450 ◽  
Female Zebrafish ◽  
Dose Dependent

AbstractOxydemeton-methyl, is an organothiophosphate insecticide, which is widely used in agricultural and urban pest controls. It exists in the environment and a large amount bioaccumulation in the wildlife due to its strong water solubility and mobility. Although its potentially harmful effect on animals and humans, few studies have focused on the oxydemeton-methyl pollution in the environment. Zebrafish have been used for many years to valuate the pollution status of water and toxicity of chemicals. In the present study, we aimed to investigate the effect of oxydemeton-methyl on the expression level of liver microsomal cytochrome P450, on the activity of NADPH-P450 reductase and reactive oxygen species (ROS) generation in zebrafish. Adult male and female zebrafish were treated with different concentration of oxydemeton-methyl (10, 50, 100 μM) for 5, 10, 20 and 30 days. We found that the oxydemeton-methyl exposure significantly increased the P450 levels and the activity of NAPDH-P450 reductase. ROS generation and the DNA damage were augmented in a dose-dependent manner in the zebrafish. These results indicated that oxydemeton-methyl is able to induce strong oxidative stress and hence highly toxic to the zebrafish.

The protects of deep sea water against photoaging of HaCaT keratinocyte induced by UVB via suppression MMPs and MAPKs/NF-κB signaling pathway

2021 ◽  
Author(s):  
Xiaolei Ma ◽  
Duomo Duan ◽  
Baolong Xie ◽  
Xunliang Wang
Keyword(s):  
Reactive Oxygen Species ◽  
Inflammatory Response ◽  
Nuclear Translocation ◽  
Sea Water ◽  
Reactive Oxygen ◽  
Collagen Degradation ◽  
Ultraviolet B ◽  
Oxygen Species ◽  
Uvb Irradiation ◽  
The Impact

Abstract Ultraviolet radiation destroys skin through several harmful effects, like inducing reactive oxygen species, inflammatory response, and collagen degradation. In this study we researched the impact of deep seawater (DSW) on the photoaging of HaCaT keratinocytes induced by ultraviolet B (UVB). DSW can inhibit epidermal hyperplasia and collagen degradation, increase skin moisture and hydroxyproline content, thereby improving the macro and histopathological damage of skin under UVB irradiation. Besides, DSW can inhibit UVB-induced oxidative stress (OS), improve antioxidant enzyme activity and inhibit the cellular signal transduction pathway of inflammatory response. Results showed DSW curbed the UVB irradiated levels of reactive oxygen species, superoxide dismutase (SOD), oxidative enzyme, glutathione peroxidase (GSH-Px), proinflammatory cytokines (TNF-α, IL-6). DSW prevented UVB-induced photoaging by suppressing collagen disorientation and expression of MMPs induced by UVB. Moreover, Western blot analyses exhibited that DSW significantly lessened the protein levels of phosphorylated SAPK/JNK kinase, phosphorylated ERK1/2 kinase, and phosphorylated p38 kinase. Similarly, UVB induced nuclear translocation of nuclear factor kappa-B were diminished by treatment of DSW. Therefore, DSW may lessen skin OS and inflammatory response under UVB irradiation. These data suggest that DSW can be used as a potentially effective skin care and dietary supplement for attenuating UVB-induced premature skin aging.

Vascular endothelial growth factor promotes sensitivity to ultraviolet B–induced cutaneous photodamage

Blood ◽  
2005 ◽  
Vol 105 (6) ◽  
pp. 2392-2399 ◽  
Author(s):  
Satoshi Hirakawa ◽  
Seishiro Fujii ◽  
Kentaro Kajiya ◽  
Kiichiro Yano ◽  
Michael Detmar
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Ultraviolet B ◽  
Epidermal Keratinocytes ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Uvb Irradiation ◽  
Uvb Exposure ◽  
Endothelial Growth Factor

AbstractAcute ultraviolet B (UVB) irradiation of the skin results in erythema, vasodilation, edema, and angiogenesis, which is associated with the expression of vascular endothelial growth factor (VEGF) by epidermal keratinocytes. It is unclear, however, whether VEGF is required for the damage or repair process that occurs in the skin on UVB exposure. We subjected transgenic mice that overexpress VEGF, and their wild-type littermates, to graded doses of acute UVB irradiation. The skin of VEGF-overexpressing mice was highly photosensitive and became erythematic when exposed to half the UVB dose required to induce erythema in wild-type mice. Erythema was associated with proliferating dermal endothelial cells, cutaneous edema, and inflammatory cell infiltration. When subjected to 10 weeks of low-level UVB irradiation, no major changes were observed in wild-type mice, whereas VEGF transgenic mice developed skin damage associated with degradation of the dermal matrix and enhanced vascularization. Systemic treatment with an anti–VEGF blocking antibody reduced the sensitivity of wild-type mice to acute UVB irradiation without inhibiting post-UVB repair. Our results reveal that VEGF promotes the cutaneous damage that occurs after UVB exposure and that the VEGF signaling pathway might serve as a novel target for the prevention of UVB-induced photodamage.

scholarly journals Astaxanthin Prevents Human Papillomavirus L1 Protein Binding in Human Sperm Membranes

Marine Drugs ◽  
2018 ◽  
Vol 16 (11) ◽  
pp. 427 ◽  
Author(s):  
Gabriella Donà ◽  
Alessandra Andrisani ◽  
Elena Tibaldi ◽  
Anna Brunati ◽  
Chiara Sabbadin ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Human Sperm ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Endogenous Reactive Oxygen Species ◽  
Anti Cancer ◽  
Anti Oxidant ◽  
L1 Protein ◽  
Gradient Separation

Astaxanthin (Asta), red pigment of the carotenoid family, is known for its anti-oxidant, anti-cancer, anti-diabetic, and anti-inflammatory properties. In this study, we evaluated the effects of Asta on isolated human sperm in the presence of human papillomavirus (HPV) 16 capsid protein, L1. Sperm, purified by gradient separation, were treated with HPV16-L1 in both a dose and time-dependent manner in the absence or presence of 30 min-Asta pre-incubation. Effects of HPV16-L1 alone after Asta pre-incubation were evaluated by rafts (CTB) and Lyn dislocation, Tyr-phosphorylation (Tyr-P) of the head, percentages of acrosome-reacted cells (ARC) and endogenous reactive oxygen species (ROS) generation. Sperm membranes were also analyzed for the HPV16-L1 content. Results show that HPV16-L1 drastically reduced membrane rearrangement with percentage of sperm showing head CTB and Lyn displacement decreasing from 72% to 15.8%, and from 63.1% to 13.9%, respectively. Accordingly, both Tyr-P of the head and ARC decreased from 68.4% to 10.2%, and from 65.7% to 14.6%, respectively. Asta pre-incubation prevented this drop and restored values of the percentage of ARC up to 40.8%. No alteration was found in either the ROS generation curve or sperm motility. In conclusion, Asta is able to preserve sperm by reducing the amount of HPV16-L1 bound onto membranes.

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