Hydrogen-rich electrolyzed warm water represses wrinkle formation against UVA ray together with type-I collagen production and oxidative-stress diminishment in fibroblasts and cell-injury prevention in keratinocytes

Author(s):  
Shinya Kato ◽  
Yasukazu Saitoh ◽  
Keizou Iwai ◽  
Nobuhiko Miwa
Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Srinivas Sriramula ◽  
Nithya Mariappan ◽  
Elizabeth McILwain ◽  
Joseph Francis

Tumor necrosis factor-alpha (TNF-α) and angiotensin II (Ang II) play an important role in the pathophysiology of cardiovascular disease in part by inducing the cardiac hypertrophic response and oxidative stress. Recently we demonstrated that angiotensin induced hypertensive response is attenuated in mice lacking the gene for TNF-α. In this study, we examined whether Ang II induced cardiac hypertrophy and increased oxidative stress is mediated through TNF-α. Methods and results: Male TNF-α (−/−) and age matched control (WT) mice were subcutaneously implanted with osmotic minipumps containing Ang II (1 μg/kg/min) or saline for 14 days. Human recombinant TNF-α was injected in one group of TNF-α (−/−) mice (10 μg/kg/day) for 14 days. In WT+Ang mice, a temporal increase in blood pressure was observed during the study as measured by radio telemetry transmitters. At the end of the study, echocardiography revealed an increase in thickness and dimensions of left ventricle (LV) and decreased fractional shortening (%FS) in WT+Ang mice. Real time RT-PCR showed that Ang II- infusion resulted in an increase in heart/bodyweight ratio and of cardiac hypertrophy markers ANP and BNP, and profibrotic genes Collagen Type I, Collagen Type II, and TGF-β in WT mice. Electron Spin resonance spectroscopy revealed an increase in total ROS, superoxide and peroxynitrite in the WT+ANG mice when compared to control WT mice. However, these changes were all attenuated in TNF-α (−/−)+Ang mice. Ang II infusion also increased significantly the mRNA expression of gp91Phox, NOX-1, NOX-4 and AT1R in the LV of WT mice, but not in TNF-α (−/−) mice. Interestingly, injection of TNF-α in the TNF-α (−/−) mice, treated with Ang II resulted in increased cardiac hypertrophy and oxidative stress. Conclusions: Findings from the present study suggest that TNF-α plays an important role in the development of cardiac hypertrophy and oxidative stress in Ang II-induced hypertension.


2004 ◽  
Vol 91 (4) ◽  
pp. 740-748 ◽  
Author(s):  
David C. Rishikof ◽  
Dennis A. Ricupero ◽  
Hanqiao Liu ◽  
Ronald H. Goldstein

2016 ◽  
Vol 6 ◽  
pp. 190-196 ◽  
Author(s):  
Haytham Jaha ◽  
Dina Husein ◽  
Yoshio Ohyama ◽  
Dongliang Xu ◽  
Shigeki Suzuki ◽  
...  

2019 ◽  
Vol 9 (8) ◽  
pp. 197 ◽  
Author(s):  
Afonso S. I. Salgado ◽  
Juliana Stramosk ◽  
Daniela D. Ludtke ◽  
Ana C. C. Kuci ◽  
Daiana C. Salm ◽  
...  

Complex regional pain syndrome type I (CRPS-I) is a chronic painful condition. We investigated whether manual therapy (MT), in a chronic post-ischemia pain (CPIP) model, is capable of reducing pain behavior and oxidative stress. Male Swiss mice were subjected to ischemia-reperfusion (IR) to mimic CRPS-I. Animals received ankle joint mobilization 48h after the IR procedure, and response to mechanical stimuli was evaluated. For biochemical analyses, mitochondrial function as well as oxidative stress thiobarbituric acid reactive substances (TBARS), protein carbonyls, antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) levels were determined. IR induced mechanical hyperalgesia which was subsequently reduced by acute MT treatment. The concentrations of oxidative stress parameters were increased following IR with MT treatment preventing these increases in malondialdehyde (MDA) and carbonyls protein. IR diminished the levels of SOD and CAT activity and MT treatment prevented this decrease in CAT but not in SOD activity. IR also diminished mitochondrial complex activity, and MT treatment was ineffective in preventing this decrease. In conclusion, repeated sessions of MT resulted in antihyperalgesic effects mediated, at least partially, through the prevention of an increase of MDA and protein carbonyls levels and an improvement in the antioxidant defense system.


2016 ◽  
Vol 311 (6) ◽  
pp. R1192-R1199 ◽  
Author(s):  
Denise C. Cornelius ◽  
Lorena M. Amaral ◽  
Kedra Wallace ◽  
Nathan Campbell ◽  
Alexia J. Thomas ◽  
...  

Preeclampsia is associated with chronic inflammation and an imbalance among T-helper cell subtypes with an increase in T-helper 17 (TH17) cells. The objective of this study was to determine a role for TH17s, from the reduced uterine perfusion pressure (RUPP) rat model of preeclampsia, in the etiology of hypertension and chronic inflammation during pregnancy. CD4+/CD25− T cells were isolated from rat spleens, cultured in TH17 media, and were verified as TH17s via flow cytometry. On day 12 of gestation, 1×106 TH17 cells from RUPP rats were adoptively transferred into NP rats, carotid catheters were inserted on day 18, and on day 19, mean arterial pressure (MAP) was recorded, serum and plasma were collected, and oxidative stress and production of agonistic autoantibodies to the ANG II type I receptor (AT1-AA) were analyzed. MAP increased from 100.3 ± 1.7 mmHg in normal pregnant (NP; n = 17) to 124.8 ± 2.1 mmHg in RUPP ( n = 22; P < 0.0001) and to 110.8 ± 2.8 mmHg in NP+RUPP TH17 ( n = 11). Pup weights in NP+RUPP TH17s were decreased to 1.92 ± 0.09 g from 2.39 ± 0.14 in NP rats ( P < 0.01). AT1-AA significantly increased from 0.1 ± 0.2 beats/min in NP to 15.6 ± 0.7 beats/min in NP+RUPP TH17s. IL-6 was 22.3 ± 5.7 pg/ml in NP and increased to 60.45 ± 13.8 pg/ml in RUPP ( P < 0.05) and 75.9 ± 6.8 pg/ml in NP+RUPP TH17 rats ( P < 0.01). Placental and renal oxidative stress were 238 ± 27.5 and 411 ± 129.9 relative light units·min−1·mg−1 in NP and 339 ± 104.6 and 833 ± 331.1 relative light units·min−1·mg−1 in NP+RUPP TH17, respectively. In conclusion, RUPP TH17 cells induced intrauterine growth restriction and increased blood pressure, AT1-AA, IL-6, and tissue oxidative stress when transferred to NP rats, indicating a role for autoimmune associated TH17 cells, to cause much of the pathophysiology associated with preeclampsia.


2019 ◽  
Vol 9 (12) ◽  
pp. 1770-1775
Author(s):  
Danhai Wu ◽  
Kan Wang

The oxidative stress process can affect bone marrow mesenchymal stem cells (BMSCs) differentiation. Interleukin (IL-15) regulates fat differentiation of BMSCs. However, the role of IL-15 in osteogenic/adipogenic differentiation of BMSCs under oxidative stress remains unclear. Rat BMSCs were cultured and randomly divided into control group; oxidative stress group and IL-15 treatment group followed by analysis of IL-15 secretion by ELISA, expression of osteocalcin, type I collagen, RUNX2 and OPN mRNA as well as FABP4 and PPARγ 2 by Real time PCR, ALP activity, ROS content and SOD activity, and expression of PI3K/Akt/mTOR signaling proteins by Western blot. In oxidative stress group, IL-15 secretion was significantly decreased, osteocalcin, type I collagen, RUNX2 and OPN mRNA expression was reduced, along with deceased ALP activity and SOD activity, increased ROS content and FABP4 and PPARγ 2 protein expression as well as decreased expression of p-AKT and mTOR in comparison of control (P < 0 05). IL-15 treatment on oxidative stress BMSCs significantly increased IL-15 secretion and the expression of osteocalcin, type I collagen, RUNX2 and OPN mRNA, along with increased ALP activity and SOD activity, decreased FABP4 and PPAR 2 protein expression and ROS content as well as increased expression of p-AKT and mTOR (P < 0 05). IL-15 secretion was reduced in BMSCs under oxidative stress. Promoting IL-15 secretion can improve redox balance through PI3K/Akt/mTOR signaling pathway, promote osteogenic differentiation of BMSCs.


PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0161479 ◽  
Author(s):  
Nathalie Mayer ◽  
Silvia Lopa ◽  
Giuseppe Talò ◽  
Arianna B. Lovati ◽  
Marielle Pasdeloup ◽  
...  

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