scholarly journals Protective effects of galangin against H2O2/UVB-induced dermal fibroblast collagen degradation via hsa-microRNA-4535-mediated TGFβ/Smad signaling

Aging ◽  
2021 ◽  
Author(s):  
Jian-Jr Lee ◽  
Shang-Chuan Ng ◽  
Yean-Tin Ni ◽  
Jian-Sheng Liu ◽  
Chih-Jung Chen ◽  
...  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shiquan You ◽  
Xiuqin Shi ◽  
Dan Yu ◽  
Dan Zhao ◽  
Quan An ◽  
...  

Abstract Background Panax notoginseng is one of the most valuable traditional Chinese medicines. Polysaccharides in P. notoginseng has been shown to significantly reduce the incidence of human diseases. However the application of fermentation technology in Panax notoginseng is not common, and the mechanism of action of P. notoginseng polysaccharides produced by fermentation is still unclear. The specific biological mechanisms of fermented P. notoginseng polysaccharides (FPNP) suppresses H2O2-induced apoptosis in human dermal fibroblast (HDF) and the underlying mechanism are not well understood. Methods In this study, the effects of water extracted and fermentation on concentration of polysaccharides in P. notoginseng extracts were analyzed. After the H2O2-induced HDF model of oxidative damage was established, and then discussed by the expression of cell markers, including ROS, MDA, SOD, CAT, GSH-Px and MMP-1, COL-I, ELN, which were detected by related ELISA kits. The expression of TGF-β/Smad pathway markers were tested by qRT-PCR to determine whether FPNP exerted antioxidant activity through TGF-β signaling in HDF cells. Results The polysaccharide content of Panax notoginseng increased after Saccharomyces cerevisiae CGMCC 17452 fermentation. In the FPNP treatment group, ROS and MDA contents were decreased, reversed the down-regulation of the antioxidant activity and expression of antioxidant enzyme (CAT, GSH-Px and SOD) induced by H2O2. Furthermore, the up-regulation in expression of TGF-β, Smad2/3 and the down-regulation in the expression of Smad7 in FPNP treated groups revealed that FPNP can inhibit H2O2-induced collagen and elastin injury by activating TGF-β/Smad signaling pathway. Conclusion It was shown that FPNP could inhibit the damage of collagen and elastin induced by H2O2 by activating the TGF-β/Smad signaling pathway, thereby protecting against the oxidative damage induced by hydrogen peroxide. FPNP may be an effective attenuating healing agent that protects the skin from oxidative stress and wrinkles.


2020 ◽  
pp. 088391152097323
Author(s):  
Dyna Susan Thomas ◽  
Chitra Manoharan ◽  
Sandhya Rasalkar ◽  
Rakesh Kumar Mishra ◽  
Ravikumar Gopalapillai

Chronic exposure to UVB radiation causes photoaging, immunosuppression, and ultimately photocarcinogenisis through the generation of reactive oxygen species (ROS). The ability of natural compounds in neutralizing the effects of oxidative stress is being explored with increased interest. Silk sericin, a biopolymer is reported to have diverse biological properties. In an effort to make the silk sericin pure, more effective and multifunctional, we have recombinantly expressed both functional sericin as well as sericin-cecropin B fusion proteins. Herein, we studied the antioxidant and anti-UVB potential of recombinant sericin and sericin-cecropin B proteins against oxidative stress using human primary dermal fibroblast cells. Treating the cells with recombinant sericin (RS) or sericin-cecropin B (RSC) prior to exposure to UVB and H2O2, effectively increased the cell viability by approximately 30% and 50%, respectively, in comparison to non-treated control. The protective effects were further evident in terms of significant reduction of LDH in oxidatively challenged cells treated with RS and RSC. A reduction in LDH release of at least 16 and 33% was observed with RS and RSC treatments, respectively, in comparison to exposed control. Further, elevated levels of catalase and superoxide dismutase (SOD) activity were observed. Importantly, the RSC fusion protein exhibited enhanced protective effects than cells treated with RS alone. Our results demonstrate that the functional attributes of cecropin B along with sericin activity in the fusion protein conferred enhanced protection against UVB- and H2O2-induced oxidative damage in human dermal fibroblasts. The improved antioxidant activity of recombinant sericin fusion biopolymer has great potential as a promising therapeutic agent for ROS-induced skin diseases.


2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Jung Hwan Oh ◽  
Jung Im Lee ◽  
Fatih Karadeniz ◽  
So Young Park ◽  
Youngwan Seo ◽  
...  

UVB exposure is one of the causes of several skin complications including but not limited to premature aging, wrinkle formation, and hyperpigmentation. UV-induced skin aging is called photoaging, and oxidative stress-induced overexpression of matrix metalloproteinases (MMPs) is the main reason behind the photoaging-mediated collagen degradation. Natural origin inhibitors of MMPs are regarded as a promising approach to prevent or treat photoaging. Therefore, the present study investigated the protective effects of 3,5-dicaffeoyl-epi-quinic acid (DCEQA) in human HaCaT keratinocytes against UVB irradiation-related dysregulation of MMPs. Changes in the mRNA and protein expression and release of MMP-1, -2, and -9 were observed after UVB irradiation with or without DCEQA treatment. In addition, the effect of DCEQA on the activation of p38, JNK, and ERK MAPKs was analyzed. Treatment of UVB-irradiated HaCaT cells with 10 μM DCEQA significantly suppressed the overexpression of both mRNA and protein of MMP-1, -2, and -9 while slightly increasing the diminished type I procollagen production. UVB-induced activation of MAPKs was also ameliorated by DCEQA treatment in a dose-dependent manner. Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production. It was suggested that DCEQA downregulated the collagen degradation via inhibition of MAPK activation, which resulted in decreased MMP activity.


2021 ◽  
Vol 8 ◽  
Author(s):  
Yan Xu ◽  
Xiaobo Qu ◽  
Jia Zhou ◽  
Guangfu Lv ◽  
Dong Han ◽  
...  

Adriamycin (ADR)-based combination chemotherapy is the standard treatment for some patients with tumors in clinical, however, long-term application can cause dose-dependent cardiotoxicity. Pilose Antler, as a traditional Chinese medicine, first appeared in the Han Dynasty and has been used to treat heart disease for nearly a thousand years. Previous data revealed pilose antler polypeptide (PAP, 3.2KD) was one of its main active components with multiple biological activities for cardiomyopathy. PAP-3.2KD exerts protective effects againt myocardial fibrosis. The present study demonstrated the protective mechanism of PAP-3.2KD against Adriamycin (ADR)-induced myocardial injury through using animal model with ADR-induced myocardial injury. PAP-3.2KD markedly improved the weight increase and decreased the HW/BW index, heart rate, and ST height in ADR-induced groups. Additionally, PAP-3.2KD reversed histopathological changes (such as disordered muscle bundles, myocardial fibrosis and diffuse myocardial cellular edema) and scores of the heart tissue, ameliorated the myocardial fibrosis and collagen volume fraction through pathological examination, significantly increased the protein level of Bcl-2, and decreased the expression levels of Bax and caspase-3 in myocardial tissue by ELISA, compared to those in ADR-induced group. Furthermore, ADR stimulation induced the increased protein levels of TGF-β1 and SMAD2/3/4, the increased phosphorylation levels of SMAD2/3 and the reduced protein levels of SMAD7. The expression levels of protein above in ADR-induced group were remarkably reversed in PAP-3.2KD-treated groups. PAP-3.2KD ameliorated ADR-induced myocardial injury by regulating the TGF-β/SMAD signaling pathway. Thus, these results provide a strong rationale for the protective effects of PAP against ADR-induced myocardial injury, when ADR is used to treat cancer.


2019 ◽  
Vol 34 (12) ◽  
pp. 1354-1362 ◽  
Author(s):  
Dongjin Noh ◽  
Jin Gyu Choi ◽  
Young Bae Lee ◽  
Young Pyo Jang ◽  
Myung Sook Oh

2018 ◽  
Author(s):  
Mohammed H Jarrar

Skin aging is a slow multifactorial process influenced by both internal as well as external factors. Ultra-violet radiations (UV), diet, smoking and personal habits are the most common environmental factors that affect skin aging. Fat contents and fibrous proteins as collagen and elastin are core internal structural components. The direct influence of UV on elastin integrity and health is central on aging of skin especially by time. The deposition of abnormal elastic material is a major marker in a photo-aged skin. Searching for compounds that may protect against cutaneous photodamage is exceedingly valued. Retinoids and alpha hydroxy acids have been endorsed by some researchers as possible candidates for protecting and or repairing the effect of UV damaged skin. For consolidating a better system of anti- and protective effects of such anti-aging agents, we evaluated the combinatory effects of various dosages of lactic acid and retinol on the dermal fibroblast’s elastin levels exposed to UV. The UV exposed cells showed significant reduction in the elastin levels. A combination of drugs with a higher concentration of lactic acid (30 -35 mM) and a lower concentration of retinol (10-15mg/mL) showed to work better in maintaining elastin concentration in UV exposed cells. We assume this preservation could be the result of increased tropo-elastin gene expression stimulated by retinol whereas lactic acid probably repaired the UV irradiated damage by enhancing the amount and integrity of the elastin fibers.


2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yo Han Hong ◽  
Ji Hye Kim ◽  
Jae Youl Cho

Ultraviolet B (UVB) radiation is the main cause of photoaging processes including cellular senescence, skin drying, collagen degradation, melanogenesis, and inflammation. These responses occur because UVB induces a change in expression of aging-related genes through regulation of signal pathways such as that of mitogen-activated protein kinases- (MAPKs-) activator protein 1 (AP-1). Ranunculus bulumei, which is used as an herb in Indonesia, belongs to the Ranunculaceae family, which has been reported to perform various physiological effects including antioxidant and anti-inflammation. However, data on the pharmaceutical and cosmeceutical utility of Ranunculus bulumei have not been reported. Therefore, we evaluated the antiaging efficacy of RB-ME, a methanol extract of Ranunculus bulumei. Rb-ME attenuated MMP9 and COX-2 gene expression but enhanced SIRT1 and type-1 collagen in UVB-irradiated HaCaT cells. Rb-ME regulated these gene expressions through inhibition of p38 phosphorylation and inactivation of AP-1. In addition, mRNA expression of HAS-2 and -3, which are involved in skin hydration, was elevated in Rb-ME-treated HaCaT cells. Rb-ME also inhibited melanogenesis by suppression of tyrosinase, MITF, and TYRP-1 mRNA in B16F10 cells under α-MSH treatment. Taken together, these results indicate that Rb-ME has a protective effect on some UVB-induced skin photoaging events such as inflammation, collagen degradation, cellular senescence, skin drying, and melanin production through inhibition of the p38-AP-1 signal cascade, indicating that Rb-ME can be used as an active ingredient for antiaging cosmetics.


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