scholarly journals Inhibition of the MAPK Signaling Pathway by Red Rice Extract in UVB-irradiated Human Skin Fibroblasts

2016 ◽  
Vol 11 (12) ◽  
pp. 1934578X1601101 ◽  
Author(s):  
Pornngarm Limtrakul ◽  
Supachai Yodkeeree ◽  
Wanisa Punfa ◽  
Jatupol Srisomboon
Keyword(s):  
Signaling Pathway ◽  
Human Fibroblasts ◽  
Radical Scavenging ◽  
Biological Properties ◽  
Mapk Signaling ◽  
Skin Aging ◽  
Mapk Signaling Pathway ◽  
Protective Effects ◽  
Red Rice ◽  
Anti Oxidant

Red rice has demonstrated several biological properties including anti-oxidant and anti-inflammation properties. However, the anti-photoaging activity has not yet been investigated. The aim of this study relates to the photo-protective effects of red rice extract (RRE) on UVB-induced skin aging. RRE was prepared and the active compounds and anti-oxidant activity were determined. The cytotoxicity of fibroblasts and secretions of IL-6 and IL-8 were evaluated. The effects of RRE on collagen and hyaluronic acid (HA) synthesis from fibroblasts were evaluated. Then, the collagenase and MMP-2 activity was determined. The effect of RRE on UV-induced MMP-1, nuclear factor kappa B (NF-κB), activator protein-1 (AP-1) and phosphorylation of MAPK protein expression was determined by western blot analysis. The RRE exerted a free radical scavenging property. RRE significantly increased collagen and HA synthesis in UVB-irradiated human fibroblasts. Moreover, RRE significantly inhibited UVB induced MMP-1 expression, MMP-2 and collagenase activity. Upon UVB irradiation, mitogen activated protein kinases (MAPKs) is activated and this pathway stimulates the expression of interleukin-6 and-8 (IL-6 and-8). Our results show that RRE decreases UVB-induced IL-6 and -8 production and the phosphorylation of c-Jun NH2-terminal kinase (JNK) and the p38 MAPK signaling process. In addition, RRE reduced UVB-induced activation of NF-κB and AP-1. RRE could suppress UV-induced inflammation and skin aging via the inhibition of the MAPK signaling pathway leading to the decrease of NF-κB and AP-1 activation resulting in a decrease in ECM degradation and an increase in ECM synthesis.

scholarly journals Photoprotective Effects of a Hyperoside-Enriched Fraction Prepared from Houttuynia cordata Thunb. on Ultraviolet B-Induced Skin Aging in Human Fibroblasts through the MAPK Signaling Pathway

Plants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2628
Author(s):  
Sariya Mapoung ◽  
Sonthaya Umsumarng ◽  
Warathit Semmarath ◽  
Punnida Arjsri ◽  
Kamonwan Srisawad ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Human Fibroblasts ◽  
Mapk Signaling ◽  
Skin Aging ◽  
Dermal Fibroblasts ◽  
Mapk Signaling Pathway ◽  
Ultraviolet B ◽  
Type I ◽  
Houttuynia Cordata ◽  
Houttuynia Cordata Thunb

Ultraviolet-B (UVB) irradiation causes skin damage via deleterious effects including oxidative stress, inflammation, and collagen degradation. The photoprotective effects of a hyperoside-enriched fraction obtained from Houttuynia cordata Thunb. (H. cordata) on the attenuation of UVB-induced skin aging in human fibroblasts were investigated. The solvent-partition technique was used to establish the hyperoside-enriched fraction of H. cordata (HcEA). The active compounds identified in the H. cordata extracts were hyperoside, quercitrin, chlorogenic acid, and rutin. With regard to the photoprotective effects of H. cordata on UVB-irradiated dermal fibroblasts, HcEA and hyperoside inhibited intracellular ROS production and inflammatory cytokine secretions (IL-6 and IL-8), while increasing collagen type I synthesis along with downregulating MMP-1 gene and protein expressions. Mechanistically, the hyperoside-enriched fraction obtained from H. cordata inhibited UVB-irradiated skin aging through regulation of the MAPK signaling pathway by attenuating the activation of JNK/ERK/c-Jun in human dermal fibroblasts. The hyperoside-enriched fraction of H. cordata exerted potent anti-skin aging properties against UVB exposure. The findings of this study can be applied in the cosmetics industry, as H. cordata extract can potentially be used in pharmaceutical or cosmetic formulations as a photoprotective or anti-skin aging agent.

scholarly journals Protective effects of alfalfa saponins on oxidative stress-induced apoptotic cells

2020 ◽  
Vol 11 (9) ◽  
pp. 8133-8140
Author(s):  
Yalei Cui ◽  
Boshuai Liu ◽  
Xiao Sun ◽  
Zidan Li ◽  
Yanyan Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Antioxidant System ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Apoptotic Cells ◽  
Protective Effects

Alfalfa saponins defend against oxidative stress by enhancing the antioxidant system and further inhibit cell apoptosis by activating the MAPK signaling pathway.

scholarly journals Cardiovascular protective effects of GLP-1:A focus on the MAPK signaling pathway

2021 ◽  
Author(s):  
Yu-Yan Zhao ◽  
Lin-Hui Chen ◽  
Liang Huang ◽  
Yong-Zhen Li ◽  
Chen Yang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Metabolic Diseases ◽  
Mapk Pathway ◽  
Signal Transduction Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Glucagon Like Peptide 1 ◽  
Common Signal

Cardiovascular and related metabolic diseases are significant global health challenges. Glucagon-like peptide 1 (GLP-1) is a brain-gut peptide secreted by ileal endocrine that is now an established drug target in type 2 diabetes (T2DM). GLP-1 targeting agents have been shown not only to treat T2DM, but also to exert cardiovascular protective effects through regulating multiple signaling pathways. The mitogen-activated protein kinase (MAPK) pathway, a common signal transduction pathway for transmitting extracellular signals to downstream effector molecules, is involved in regulating diverse cell physiological processes, including cell proliferation, differentiation, stress, inflammation, functional synchronization, transformation and apoptosis. The purpose of this review is to highlight the relationship between GLP-1 and cardiovascular disease (CVD), and discuss how GLP-1 exerts cardiovascular protective effects through MAPK signaling pathway. This review also discusses the future challenges in fully characterizing and evaluating the CVD protective effects of GLP-1 receptor agonists (GLP-1RA) at the cellular and molecular level. A better understanding of MAPK signaling pathway that are disregulated in CVD may aid in the design and development of promising GLP-1RA.

scholarly journals Eckol Inhibits Particulate Matter 2.5-Induced Skin Keratinocyte Damage via MAPK Signaling Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (8) ◽  
pp. 444 ◽  
Author(s):  
Ao Xuan Zhen ◽  
Yu Jae Hyun ◽  
Mei Jing Piao ◽  
Pincha Devage Sameera Madushan Fernando ◽  
Kyoung Ah Kang ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Signaling Pathway ◽  
Cell Damage ◽  
Brown Seaweed ◽  
Underlying Mechanism ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Ros Generation ◽  
Protective Effects ◽  
Skin Damage

Toxicity of particulate matter (PM) towards the epidermis has been well established in many epidemiological studies. It is manifested in cancer, aging, and skin damage. In this study, we aimed to show the mechanism underlying the protective effects of eckol, a phlorotannin isolated from brown seaweed, on human HaCaT keratinocytes against PM2.5-induced cell damage. First, to elucidate the underlying mechanism of toxicity of PM2.5, we checked the reactive oxygen species (ROS) level, which contributed significantly to cell damage. Experimental data indicate that excessive ROS caused damage to lipids, proteins, and DNA and induced mitochondrial dysfunction. Furthermore, eckol (30 μM) decreased ROS generation, ensuring the stability of molecules, and maintaining a steady mitochondrial state. The western blot analysis showed that PM2.5 promoted apoptosis-related protein levels and activated MAPK signaling pathway, whereas eckol protected cells from apoptosis by inhibiting MAPK signaling pathway. This was further reinforced by detailed investigations using MAPK inhibitors. Thus, our results demonstrated that inhibition of PM2.5-induced cell apoptosis by eckol was through MAPK signaling pathway. In conclusion, eckol could protect skin HaCaT cells from PM2.5-induced apoptosis via inhibiting ROS generation.

scholarly journals MSCs enhances the protective effects of valsartan on attenuating the doxorubicin-induced myocardial injury via AngII/NOX/ROS/MAPK signaling pathway

Aging ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 22556-22570
Author(s):  
Dong Cheng ◽  
Wencheng Tu ◽  
Libo Chen ◽  
Haoren Wang ◽  
Qinfu Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Myocardial Injury ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Protective Effects

scholarly journals Melatonin Protects TEGDMA induced Pre-odontoblasts Mitochondrial Apoptosis via JNK/MAPK Signaling Pathway

2021 ◽  
Author(s):  
Qihao Yu ◽  
Yi Liu ◽  
Konghuai Wang ◽  
Xunben Weng ◽  
Shengbin Huang ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Dental Pulp ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Protective Effects ◽  
Mitochondrial Apoptosis ◽  
Atp Level ◽  
Induced Apoptosis

Abstract Background: Resin monomer induced dental pulp injury presents a mitochondrial dysfunction related pathology. Melatonin has been regarded as a strong mitochondrial protective bioactive compound from pineal gland. However, it remains unknown whether melatonin can prevent dental pulp from resin monomer induced injury. The aim of the study is to investigate the effects of melatonin on TEGDMA, a major component in dental resin, induced mouse pre-odontoblast cell lines (mDPC6T) mitochondrial apoptosis and to verify whether JNK/MAPK signaling pathway mediate the protective effect of melatonin. Methods: We adopted a well-established TEGDMA-induced mDPC6T apoptosis model to investigate the preventive effect of melatonin by detecting cell viability, apoptosis rate, expression of apoptosis related protein, mitochondrial ROS (mtROS) production, mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) level. Inhibitors of MAPKs signaling were used to explore which pathway was participated in TEGDMA induced apoptosis. Finally, we verified the role of JNK/MAPK pathway during the protective effects of melatonin above by the agonist and antagonists of JNK.Results: Melatonin attenuated TEGDMA induced mDPC6T apoptosis via reducing mtROS production, rescuing MMP and ATP level. Meanwhile, the mitochondrial dysfunction and apoptosis was alleviated by the JNK/MAPK inhibitor SP600125 but not the other MAPKs signaling inhibitors. Furthermore, melatonin down-regulated the expression of phosphorylated-JNK, and eliminated the active effects of Anisomycin on JNK/MAPK pathway, which mimicked the effects of the SP600125.Conclusion: Our findings demonstrated that melatonin protected mDPC6T against TEGDMA induced apoptosis via JNK/MAPK signaling and maintenance of mitochondrial function, which presented a novel therapeutic strategy for prevention against resin monomer-induced dental pulp injury.

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