scholarly journals Photoprotective Effects of Sargassum Thunbergii on Ultraviolet B-Induced Mouse L929 Fibroblasts and Zebrafish

2021 ◽  
Author(s):  
Bei Chen ◽  
Honghong Chen ◽  
Haidong Qu ◽  
Kun Qiao ◽  
Min Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Inflammatory Cytokine ◽  
Dna Condensation ◽  
Ultraviolet B ◽  
Uvb Radiation ◽  
Sargassum Thunbergii ◽  
L929 Cells ◽  
Mda Content

Abstract Background: Chronic exposure to ultraviolet B (UVB) causes a series of adverse skin reactions, such as erythema, sunburn, photoaging, and cancer, by altering signaling pathways related to inflammation, oxidative stress, and DNA damage. Marine algae have abundant amounts and varieties of bioactive compounds that possess antioxidant and anti-inflammatory properties. Thus, the objective of this study was to investigate the photoprotective effects of an ethanol extract of Sargassum thunbergii.Methods: Sargassum thunbergii phenolic-rich extract (STPE) was prepared, and its activity against UVB damage was evaluated using L929 fibroblast cells and zebrafish. STPE was extracted and purified by 40% ethanol and macroporous resin XDA-7. Reactive oxygen species (ROS) and antioxidant markers, such as superoxide dismutase (SOD), catalase (CAT) activities, and malondialdehyde (MDA) content were analyzed. The effect of STPE on UVB-induced inflammation was determined by inflammatory cytokine gene and protein expression. The expression of signaling molecules in the Nuclear Factor KappaB (NF-κB) pathway was determined by western blotting. DNA condensation was analyzed and visualized by Hoechst 33342 staining. In vivo evaluation was performed by tail fin area and ROS measurement using the zebrafish model. Results: The total polyphenol content of STPE was 72%. STPE reduced ROS content in L929 cells, improved SOD and CAT activities, and significantly reduced MDA content, thereby effectively alleviating UVB radiation-induced oxidative damage. STPE inhibited the mRNA and protein expression of TNF-α, IL-6, and IL-1α. STPE reversed DNA condensation at concentrations of 20 and 40 μg/mL compared with the UVB control. Moreover, STPE inhibited NF-κB signaling pathway activation and alleviated DNA agglutination in L929 cells after UVB irradiation. Additionally, 1.67 μg/mL STPE significantly increased the tail fin area in zebrafish, and 0.8–1.6 μg/mL STPE effectively eliminated excessive ROS after UVB radiation. Conclusions: STPE inhibited UVB-induced oxidative stress, inflammatory cytokine expression, and DNA condensation via downregulation of the NF-κB signaling pathway, suggesting that it prevents UVB-induced cell damage and photoaging, and has potential for clinical development for skin disease treatment.

Protective Effects of Ginsenosides on 17α-Ethynyelstradiol-Induced Intrahepatic Cholestasis via Anti-Oxidative and Anti-Inflammatory Mechanisms in Rats

2017 ◽  
Vol 45 (08) ◽  
pp. 1613-1629 ◽  
Author(s):  
Yan-Jiao Xu ◽  
Zao-Qin Yu ◽  
Cheng-Liang Zhang ◽  
Xi-Ping Li ◽  
Cheng-Yang Feng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alkaline Phosphatase ◽  
Superoxide Dismutase ◽  
Protein Expression ◽  
Intrahepatic Cholestasis ◽  
Serum Levels ◽  
Total Bile Acid ◽  
Protective Effects ◽  
Sod Activity ◽  
Mda Content

The present study was designed to assess the effects and potential mechanisms of ginsenosides on 17[Formula: see text]-ethynyelstradiol (EE)-induced intrahepatic cholestasis (IC). Ginsenoside at doses of 30, 100, 300[Formula: see text]mg/kg body weight was intragastrically (i.g.) given to rats for 5 days to examine the effect on EE-induced IC. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bile acid (TBA) were measured. Hepatic malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. Protein expression of proinflammatory cytokines TNF-[Formula: see text], IL-6 and IL-1[Formula: see text] was analyzed by immunohistochemistry and Western blot. Results indicated that ginsenosides remarkably prevented EE-induced increase in the serum levels of AST, ALT, ALP and TBA. Moreover, the elevation of hepatic MDA content induced by EE was significantly reduced, while hepatic SOD activities were significantly increased when treated with ginsenosides. Histopathology of the liver tissue showed that pathological injuries were relieved after treatment with ginsenosides. In addition, treatment with ginsenosides could significantly downregulate the protein expression of TNF-[Formula: see text], IL-6 and IL-1[Formula: see text] compared with EE group. These findings indicate that ginsenosides exert the hepatoprotective effect on EE-induced intrahepatic cholestasis in rats, and this protection might be attributed to the attenuation of oxidative stress and inflammation.

scholarly journals PO-086 Exercise enhances cardiac antioxidant capacity in diabetic rats through the Keap1/Nrf2 signaling pathway

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Shiqiang Wang
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Diabetic Rats ◽  
Heart Weight ◽  
Stress Injury ◽  
Myocardial Oxidative Stress ◽  
Nrf2 Signaling Pathway ◽  
Gene And Protein Expression

Objective To investigate the effects of exercise on the myocardial oxidative stress injury of diabetic rats, and discussed the role of Keap1/Nrf2 signaling pathway in this process Methods  Tyep 2 diabetic rat model was established by streptozotocin injection through abdominal cavity and high fat diet. The all the diabetic rats were divided into three groups: control group (NC), diabetes group(T2DM) and diabetes exercise group, NC and T2DM group were kept quiet for 8 weeks, T2DME group was trained for 8 weeks. After the exercise, weight, heart weight and blood were measured. MDA, T-SOD and GSH-PX enzyme were measured by biochemical method. Ho-1, Keap1, Nrf2 gene and protein expression were detected by RT-PCR and WesternBlotting. Results Compared with NC group, the weight of rats in the T2DM group significantly decreased [(528+/-71g vs 362+/-33g), P<0.05], HWI  significantly increased [(2.845+/-0.22 vs 3.841+/-0.21, P <0.05], blood glucose was significantly increased [(6.4±3.8 vs 26±7.5mmol/L), P <0.01],T-SOD and GSH-PX activity decreased significantly (P<0.05), Ho-1 protein expression increased (P<0.01), Keap1 and Nrf2 showed no significant changes, and Nrf2 nuclear transposition decreased (P<0.05). Compared with the T2DM group, no significant change in body weight and heart weight in the T2DME group, with significant decrease in HWI[（3.841±0.21 vs 3.235±0.23），P＜0.05], with significant decrease in blood glucose [（26.0±7.5 vs 21.0±6.8），P＜0.05]. Ho-1 gene and protein expression increased significantly（P＜0.05and P＜0.01）, with no significant change of Keap1, while Nrf2 expression increased significantly (P < 0.05), and Nrf2 nuclear transposition increased significantly (P < 0.01). Conclusions Exercise activates the myocardial Keap1/Nrf2 signaling pathway in rats, promotes the expression of downstream antioxidant enzymes, increases cardiac antioxidant capacity, and resists diabetic myocardial oxidative stress injury.

scholarly journals The Effect and Mechanism of KLF7 in the TLR4/NF-κB/IL-6 Inflammatory Signal Pathway of Adipocytes

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Meixiu Zhang ◽  
Cuizhe Wang ◽  
Jinxiu Wu ◽  
Xiaodan Ha ◽  
Yuchun Deng ◽  
...  
Keyword(s):  
Protein Expression ◽  
Signaling Pathway ◽  
Transcriptional Activation ◽  
Inflammatory Cytokine ◽  
Luciferase Reporter ◽  
Signal Pathways ◽  
High Concentration ◽  
Inflammatory Signaling ◽  
Expression Levels ◽  
Mrna And Protein Expression

Objective. To investigate the role and possible molecular mechanism of Krüppel-like factor 7 (KLF7) in the TLR4/NF-κB/IL-6 inflammatory signaling pathway activated by free fatty acids (FFA). Methods. The mRNA and protein expression levels of KLF7 and the factors of TLR4/NF-κB/IL-6 inflammatory signal pathways were detected by qRT-PCR and Western blotting after cell culture with different concentrations of palmitic acid (PA). The expression of KLF7 or TLR4 in adipocytes was upregulated or downregulated; after that, the mRNA and protein expression levels of these key factors were detected. KLF7 expression was downregulated while PA stimulated adipocytes, and then the mRNA and protein expressions of KLF7/p65 and downstream inflammatory cytokine IL-6 were detected. The luciferase reporter assay was used to determine whether KLF7 had a transcriptional activation effect on IL-6. Results. (1) High concentration of PA can promote the expression of TLR4, KLF7, and IL-6 in adipocytes. (2) TLR4 positively regulates KLF7 expression in adipocytes. (3) KLF7 positively regulates IL-6 expression in adipocytes. (4) PA promotes IL-6 expression via KLF7 in adipocytes. (5) KLF7 has a transcriptional activation on IL-6. Conclusion. PA promotes the expression of the inflammatory cytokine IL-6 by activating the TLR4/KLF7/NF-κB inflammatory signaling pathway. In addition, KLF7 may directly bind to the IL-6 promoter region and thus activate IL-6.

scholarly journals Melatonin and Its Metabolites Ameliorate UVR-Induced Mitochondrial Oxidative Stress in Human MNT-1 Melanoma Cells

2018 ◽  
Vol 19 (12) ◽  
pp. 3786 ◽  
Author(s):  
Konrad Kleszczyński ◽  
Bernadetta Bilska ◽  
Agatha Stegemann ◽  
Damian Flis ◽  
Wieslaw Ziolkowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Phosphorylation ◽  
Melanoma Cells ◽  
Ultraviolet B ◽  
Melatonin Receptors ◽  
Biologically Active ◽  
Uvb Radiation ◽  
Mitochondrial Oxidative Stress ◽  
Uncoupling Of Oxidative Phosphorylation ◽  
Uvb Exposure

Melatonin (Mel) is the major biologically active molecule secreted by the pineal gland. Mel and its metabolites, 6-hydroxymelatonin (6(OH)Mel) and 5-methoxytryptamine (5-MT), possess a variety of functions, including the scavenging of free radicals and the induction of protective or reparative mechanisms in the cell. Their amphiphilic character allows them to cross cellular membranes and reach subcellular organelles, including the mitochondria. Herein, the action of Mel, 6(OH)Mel, and 5-MT in human MNT-1 melanoma cells against ultraviolet B (UVB) radiation was investigated. The dose of 50 mJ/cm2 caused a significant reduction of cell viability up to 48%, while investigated compounds counteracted this deleterious effect. UVB exposure increased catalase activity and led to a simultaneous Ca++ influx (16%), while tested compounds prevented these disturbances. Additional analysis focused on mitochondrial respiration performed in isolated mitochondria from the liver of BALB/cJ mice where Mel, 6(OH)Mel, and 5-MT significantly enhanced the oxidative phosphorylation at the dose of 10−6 M with lower effects seen at 10−9 or 10−4 M. In conclusion, Mel, 6(OH)Mel and 5-MT protect MNT-1 cells, which express melatonin receptors (MT1 and MT2) against UVB-induced oxidative stress and mitochondrial dysfunction, including the uncoupling of oxidative phosphorylation.

scholarly journals Effect of Lactobacillus reuteri Administration on Wrinkle Formation and Type I Procollagen Levels in UVB-Exposed Male Balb/c Mice (Mus musculus)

2020 ◽  
Vol 4 (3) ◽  
pp. 113
Author(s):  
Ivanna Valentina ◽  
Achadiyani Achadiyani ◽  
Sunarjati Sudigdo Adi ◽  
Ronny Lesmana ◽  
Reni Farenia
Keyword(s):  
Oxidative Stress ◽  
Lactobacillus Reuteri ◽  
Ultraviolet B ◽  
Type I ◽  
Uvb Radiation ◽  
Dorsal Skin ◽  
Uvb Irradiation ◽  
Type I Procollagen ◽  
Group 3 ◽  
Group 1

Background: Chronic Ultraviolet B (UVB) exposure causes oxidative stress that may induce damages to the collagen matrix and thus plays a role in the wrinkle formation. Lactobacillus reuteri is a probiotic that may exerts antioxidant effects, thus helping to reduce damages caused by UVB-induced oxidative stress in the skin.Materials and Methods: Twenty-eight male Balb/c mice were divided equally into control group, UVB radiation only group, oral L. reuteri supplementation only group, and UVB radiation with oral L. reuteri supplementation group. UVB irradiation was given 3 times a week (100 seconds/exposure, within 3 cm distance) for 10 weeks, with a total dose of 166 mJ/cm2. Oral L. reuteri supplementation (0.2 mL, 108 CFU) was provided every morning after meal via orogastric feeding tube for 10 weeks. Wrinkle formation on the dorsal skin of the mice was evaluated in accordance with the Bissett method and type I procollagen levels was evaluated by western blotting.Results: In comparison with the group receiving only UVB irradiation, the group receiving probiotic and UVB irradiation showed significantly lower wrinkle scores (Group 1 vs. Group 3, 2.50±0.55 vs. 1.00±0,00; p<0.05) and significantly higher type I procollagen levels (Group 1 vs. Group 3, 0.88±0.36 vs. 1.92±0.46; p<0.05).Conclusion: Results of the current study showed that L. reuteri supplementation may reduce wrinkle formation and increase type I procollagen production in UVB-exposed dorsal skin of male Balb/c mice.Keywords: Lactobacillus reuteri, type I procollagen, photoaging, wrinkles, ultraviolet B

scholarly journals Horse Oil Mitigates Oxidative Damage to Human HaCaT Keratinocytes Caused by Ultraviolet B Irradiation

2019 ◽  
Vol 20 (6) ◽  
pp. 1490
Author(s):  
Mei Piao ◽  
Kyoung Kang ◽  
Ao Zhen ◽  
Hee Kang ◽  
Young Koh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Matrix Metalloproteinase ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Ultraviolet B ◽  
Electromagnetic Spectrum ◽  
Oxygen Species ◽  
Uvb Radiation ◽  
Hacat Keratinocytes

Horse oil products have been used in skin care for a long time in traditional medicine, but the biological effects of horse oil on the skin remain unclear. This study was conducted to evaluate the protective effect of horse oil on ultraviolet B (UVB)-induced oxidative stress in human HaCaT keratinocytes. Horse oil significantly reduced UVB-induced intracellular reactive oxygen species and intracellular oxidative damage to lipids, proteins, and DNA. Horse oil absorbed light in the UVB range of the electromagnetic spectrum and suppressed the generation of cyclobutane pyrimidine dimers, a photoproduct of UVB irradiation. Western blotting showed that horse oil increased the UVB-induced Bcl-2/Bax ratio, inhibited mitochondria-mediated apoptosis and matrix metalloproteinase expression, and altered mitogen-activated protein kinase signaling-related proteins. These effects were conferred by increased phosphorylation of extracellular signal-regulated kinase 1/2 and decreased phosphorylation of p38 and c-Jun N-terminal kinase 1/2. Additionally, horse oil reduced UVB-induced binding of activator protein 1 to the matrix metalloproteinase-1 promoter site. These results indicate that horse oil protects human HaCaT keratinocytes from UVB-induced oxidative stress by absorbing UVB radiation and removing reactive oxygen species, thereby protecting cells from structural damage and preventing cell death and aging. In conclusion, horse oil is a potential skin protectant against skin damage involving oxidative stress.

scholarly journals Glutamine Improves Oxidative Stress through the Wnt3a/β-Catenin Signaling Pathway in Alzheimer’s Disease In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Yuan Wang ◽  
Qiang Wang ◽  
Jie Li ◽  
Gang Lu ◽  
Zhibin Liu
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Stress Injury ◽  
Mda Content ◽  
Samp8 Mice

Background/Aims. Alzheimer’s disease (AD) is the most common neurodegenerative disease, and all researchers working in this field agree that oxidative stress is intimately associated with Alzheimer disease. In this study, we hypothesized that glutamine (Gln) offers protection against oxidative stress injury in SAMP8 mice as well as the underlying mechanism. Methods. The SAMP8 mice received glutamine intragastrically for 8 consecutive weeks to evaluate the protective effect of glutamine on oxidative stress in AD mice involving Wnt3a/β-catenin signaling pathway. In addition, rat pheochromocytoma tumor cell line PC12 was pretreated with 32 μM glutamine for 2 h followed by 24 h incubation with 40 μM Aβ25-35 to obtain in vitro data. Results. In vivo the administration of glutamine was found to ameliorate behavioral deficits and neuron damage, increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-XP) activity, reduce the malondialdehyde (MDA) content, and activate the Wnt3a/β-catenin signaling pathway in SAMP8 mice. In vitro glutamine treatment decreased the toxicity of Aβ25-35 on PC12 cells and prevented apoptosis. Additionally, glutamine treatment increased SOD and GSH-XP activity and decreased MDA content and increased Wnt3a and β-catenin protein levels. Interestingly, the DKK-1 (Wnt3a/β-catenin pathway inhibitor) decreased the antioxidant capacity of glutamine in Aβ25-35-treated PC12 cells. Conclusion. This study suggests that glutamine could protect against oxidative stress-induced injury in AD mice via the Wnt3a/β-catenin signaling pathway.

scholarly journals Protective Effect of Curcumin Against Oxidative Stress-Induced Injury in Rats with Parkinson’s Disease Through the Wnt/ β-Catenin Signaling Pathway

2017 ◽  
Vol 43 (6) ◽  
pp. 2226-2241 ◽  
Author(s):  
Yun-Liang Wang ◽  
Bo Ju ◽  
Yu-Zhen Zhang ◽  
Hong-Lei Yin ◽  
Ya-Jun Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Tunel Staining ◽  
Primary Cells ◽  
Mda Content ◽  
6 Hydroxydopamine ◽  
Dickkopf 1

Background/Aims: The study aimed to investigate the protective effect of curcumin against oxidative stress-induced injury of Parkinson’s disease (PD) through the Wnt/β-catenin signaling pathway in rats. Methods: The successfully established PD rat models and normal healthy rats were randomly assigned into the 6-hydroxydopamine (6-OHDA), the curcumin (Cur) and the control groups. Immunohistochemistry was used to detect the positive expression of tyrosine hydroxylase (TH), dopamine transporter (DAT) and glial fibrillary acidic protein (GFAP). Deutocerebrum primary cells were extracted and classified into the control, 6-OHDA, Cur (5, 10, 15 µmol/L), Dickkopf-1 (DKK-1) and Cur + DKK-1 groups. MTT assays, adhesion tests and TUNEL staining were used to assess cell viability, adhesion and apoptosis, respectively. Western blotting and qRT-PCR were used to examine the protein and mRNA expressions of Wnt3a and β-catenin and the c-myc and cyclinD1 mRNA expressions. Results: TH and DAT expressions in the Cur group were elevated and GFAP was reduced compared with the 6-OHDA group. Curcumin enhanced viability, survival and adhesion and attenuated apoptosis of deutocerebrum primary cells by activating the Wnt/β-catenin signaling pathway. Higher Wnt3a and β-catenin mRNA and protein expressions and c-myc and cyclinD1 mRNA expressions, enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) contents, decreased malondialdehyde (MDA) content and elevated mitochondrial membrane potential (∆ψm) were found in the 10 and 15 µmol/L Cur groups compared with the 6-OHDA group. However, opposite tendencies were found in the Cur + DKK-1 group compared to the 10 µmol/L Cur group. Conclusion: This study suggests that curcumin could protect against oxidative stress-induced injury in PD rats via the Wnt/β-catenin signaling pathway.

scholarly journals PO-167 Effects of Hydrogen-rich Water on Rat Skeletal Muscles' Oxidative Damage and Autophagy Induced by Repeated Exhaustive Exercise

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Zujie Xu ◽  
Hongdi Gu ◽  
Zhenjun Tian
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Protein Expression ◽  
Muscle Tissue ◽  
Skeletal Muscle Tissue ◽  
Exhaustive Exercise ◽  
Ultrastructural Changes ◽  
Sod Activity ◽  
Hydrogen Water ◽  
Mda Content

Objective This study was carried out to detect the effects of hydrogen-water intervention on oxidative stress and cell autophagy in skeletal muscle of rats with repeated exhaustion.  Methods 30 male SD rats in the age of 3 months, weighing 180-210g, were randomly divided into control group (C), repeated exhaustion group (EX), and the repeated exhaustion with hydrogen intervention group (EH), 10 rats in each group. The EX and EH groups were subjected to a four-weeks of repeated-exhaustive exercise. The initial speed of the exercise was 15 m/min, and increasedby 5 m/min every 5 min, the final speed is 35m/min until  exhaustion, 5 d/wk, with a total of 4 wk. In EH group, hydro-water was given to rats 30 mins before exercise. The ultrastructural changes of skeletal muscle were observed by using a transmission electron microscopy. Activity of SDH and CK in serum and SOD activity, MDA content and T-AOC level in skeletal muscle tissue were detected. Western blotting was used to detect the proteins expression of autophagy related proteins in skeletal muscle, mTOR, p-mTOR, LC3B-2 and P53.  Results Compared with the EX group, in the EH group, the ultrastructural damage and mitochondrial swelling were significantly reduced, and the time of exhaustion was significantly prolonged (p<0.05), Serum SDH activity increased significantly (p<0.05), CK activity decreased significantly (p<0.05), and skeletal muscle tissue SOD activity and total antioxidant capacity significantly increased (p<0.05), MDA content decreased significantly (p<0.01), mTOR and p-mTOR protein expression was significantly increased(p<0.05), the LC3B-2 and P53 protein expression was significantly lower (p<0.05). Conclusions Hydrogen water intervention could significantly improve repeatedly exhaustion exercise result in rat skeletal muscle injury, oxidative stress and cell ultrastructure damage excessive autophagy, improving oxidation resistance of the skeletal muscle and exercise endurance.

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