Cordyceps militaris Extract Protects Human Dermal  Fibroblasts against Oxidative Stress-Induced Apoptosis  and Premature Senescence

Park, Jun Myoung; Lee, Jong Seok; Lee, Ki Rim; Ha, Suk‐Jin; Hong, Eock Kee

doi:10.3390/nu6093711

Cited by 33 publications

(22 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tumor necrosis factor alpha (TNF-α) and hydrogen peroxide (H 2 O 2 ), which induce apoptosis through extrinsic and intrinsic pathways, respectively, have been shown to induce fibroblast apoptosis (Boucher and others 2010; Niederer and others 2012; Park and others 2014; Szigeti and others 2010; Zhang and others 2011). To confirm that fibroblasts from the lung of old mice are more resistant to apoptosis and fibrogenic than fibroblasts from young mice, lung fibroblasts were isolated from 3- and 22-month old mice and treated with H 2 O 2 , TNF-α, or TGF-β1.…”

Section: Resultsmentioning

confidence: 99%

Plasminogen activator inhibitor 1, fibroblast apoptosis resistance, and aging-related susceptibility to lung fibrosis

Huang

Akhter

Jiang

et al. 2015

Experimental Gerontology

View full text Add to dashboard Cite

Idiopathic pulmonary fibrosis (IPF) is a fatal lung disorder with unknown cause and no effective treatment. The incidence of and mortality from IPF increase with age, suggesting that advanced age is a major risk factor for IPF. The mechanism underlying the increased susceptibility of the elderly to IPF, however, is unknown. In this study, we show for the first time that the protein level of plasminogen activator inhibitor 1 (PAI-1), a protease inhibitor which plays an essential role in the control of fibrinolysis, was significantly increased with age in mouse lung homogenate and lung fibroblasts. Upon bleomycin challenge, old mice experienced augmented PAI-1 induction and lung fibrosis as compared to young mice. Most interestingly, we show that fewer (myo)fibroblasts underwent apoptosis and more (myo)fibroblasts with increased level of PAI-1 accumulated in the lung of old than in young mice after bleomycin challenge. In vitro studies further demonstrate that fibroblasts isolated from lungs of old mice were resistant to H2O2 and tumor necrosis factor alpha-induced apoptosis and had augmented fibrotic responses to TGF-β1, compared to fibroblasts isolated from young mice. Inhibition of PAI-1 activity with a PAI-1 inhibitor, on the other hand, eliminated the aging-related apoptosis resistance and TGF-β1 sensitivity in isolated fibroblasts. Moreover, we show that knocking down PAI-1 in human lung fibroblasts with PAI-1 siRNA significantly increased their sensitivity to apoptosis and inhibited their responses to TGF-β1. Together, the results suggest that increased PAI-1 expression may underlie the aging-related sensitivity to lung fibrosis in part by protecting fibroblasts from apoptosis.

show abstract

Section: Resultsmentioning

confidence: 99%

Plasminogen activator inhibitor 1, fibroblast apoptosis resistance, and aging-related susceptibility to lung fibrosis

Huang

Akhter

Jiang

et al. 2015

Experimental Gerontology

View full text Add to dashboard Cite

show abstract

“…literature has been published on in vitro models of HDFs for the study of aging (Park et al, 2014). Fibroblasts are vital cellular components of human skin as they play essential roles in the regulation of skin physiology and pathology.…”

Section: Discussionmentioning

confidence: 99%

Combined extract of Moringa oleifera and Centella asiatica modulates oxidative stress and senescence in hydrogen peroxide-induced human dermal fibroblasts

Hisam¹,

Rofiee²,

Khalid³

et al. 2018

Turk J Biol

View full text Add to dashboard Cite

Moringa oleifera Lam. and Centella asiatica (L.) Urb. leaves have been previously reported to exhibit antioxidant activity. The objective of the present study is to determine the in vitro antioxidant activity of the combined extracts of M. oleifera and C. asiatica (TGT-PRIMAAGE) and its effect on hydrogen peroxide (H 2 O 2)-induced oxidative stress in human dermal fibroblasts. TGT-PRIMAAGE acted on the mechanism of hydrogen transfer as it showed scavenging activity in the DPPH assay. This is due to the presence of phenolics and flavonoids in TGT-PRIMAAGE. TGT-PRIMAAGE effectively reduced cellular generation of reactive oxygen species induced by H 2 O 2. The activities of superoxide dismutase and catalase were also increased in cells treated with TGT-PRIMAAGE. Treatment with TGT-PRIMAAGE showed significant reduction (P < 0.05) in the number of senescent cells. Significant reduction (P < 0.05) of malondialdehyde was also seen in cells treated with TGT-PRIMAAGE. The p53 protein level was reduced in TGT-PRIMAAGEtreated cells, which indicates its potential in protecting the cells from oxidative stress induced by H 2 O 2 .

show abstract

“…Mitochondrial electron transport chain, NADPH oxidases (Noxes) and uncoupled nitric oxide synthase are the major sources of hydrogen peroxide (H 2 O 2 ) in vessel walls [26][27][28]. It is well established that reaction of vascular-bound MPO with H 2 O 2 can produce more potent vascular injury species, such as HOCl and chlorinating species, which represent an important injury pathway in diabetic vascular damage.…”

Section: Discussionmentioning

confidence: 99%

Role of vascular peroxidase 1 in senescence of endothelial cells in diabetes rats

Liu

Yuan

et al. 2015

International Journal of Cardiology

View full text Add to dashboard Cite

Cordyceps militaris Extract Protects Human Dermal Fibroblasts against Oxidative Stress-Induced Apoptosis and Premature Senescence

Cited by 33 publications

References 42 publications

Plasminogen activator inhibitor 1, fibroblast apoptosis resistance, and aging-related susceptibility to lung fibrosis

Plasminogen activator inhibitor 1, fibroblast apoptosis resistance, and aging-related susceptibility to lung fibrosis

Combined extract of Moringa oleifera and Centella asiatica modulates oxidative stress and senescence in hydrogen peroxide-induced human dermal fibroblasts

Role of vascular peroxidase 1 in senescence of endothelial cells in diabetes rats

Contact Info

Product

Resources

About