Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose

Mao, Genxiang; Zheng, Ling-Di; Cao, Yong-Bao; Chen, Zhuo-Mei; Lv, Yuandong; Wang, Yazhen; Hu, Xiao; Wang, Guofu; Yan, Jing

doi:10.1155/2012/750963

Cited by 55 publications

(41 citation statements)

References 31 publications

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“…Serum superoxide dismutase (SOD) and malondialdehyde (MDA) were evaluated according to respective ELISA kits (Nanjing Jiancheng Bioengineering Institute, Nanjing, China) as described [21]. Briefly, the level of SOD was assessed by xanthine-xanthine oxidase system to produce superoxide ions, which reacted with 2-(4-iodophenyl)-3-(4-nitrophenol-5-phenlyltetrazolium chloride) to form red formazan dye, and the final products at 550 nm were measured.…”

Section: Measurement Of Ros Generationmentioning

confidence: 99%

Improvement of Huangqi Decoction on Endothelial Dysfunction in 5/6 Nephrectomized Rats

Chu

Wang

Mao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Endothelial dysfunction is a major factor in the progression of chronic kidney disease, which correlates with oxidative stress and NO deficiency. Huangqi decoction (HQD) is a potential anti-oxidant ingredient in renoprotection. However, the underlying mechanisms remained identified. Therefore, we investigated whether HQD exhibit improvement in endothelial dysfunction in the 5/6 nephrectomy (Nx) rat model. Methods: Male Wistar rats (180 - 250 g) were divided into sham, Nx and Nx + HQD (0.05, 0.15 and 0.45 g/kg) group, respectively. Renal function and histology were examined with ELISA and Immunohistochemical analysis. Endothelium-dependent relaxation of rat aortas was investigated by isometric tension recordings. Oxidative stress and NO bioavailability were detected by ELISA, DHE-staining, DAF-2 staining and western blotting. Results: Compared with Nx rats, HQD treatment reversed the functional and structural changes of kidney significantly. Besides, endothelium-dependent relaxation of rat aortas was also improved by HQD treatment. NADPH oxidase and ROS generation were inhibited while NO bioavailability was enhanced. Conclusion: HQD can act as a potent prescription for the treatment of endothelium related vascular complications.

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Section: Measurement Of Ros Generationmentioning

confidence: 99%

Improvement of Huangqi Decoction on Endothelial Dysfunction in 5/6 Nephrectomized Rats

Chu

Wang

Mao

et al. 2016

Cell Physiol Biochem

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“…Epithelial cells forming tight junctions appear to reach higher CI values than fibroblasts. Caco-2 cells reached a CI of 5 [27], HUVEC of 6 [28], while diploid fetal fibroblasts reached 3.5 [29]. …”

Section: Discussionmentioning

confidence: 99%

Suitability of Cell-Based Label-Free Detection for Cytotoxicity Screening of Carbon Nanotubes

Meindl

Absenger

Roblegg

et al. 2013

BioMed Research International

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Cytotoxicity testing of nanoparticles (NPs) by conventional screening assays is often complicated by interference. Carbon nanotubes (CNTs) are particularly difficult to assess. To test the suitability of cell-based label-free techniques for this application, a panel of CNTs with different diameters and surface functionalizations was assessed by impedance-based technique (xCELLigence RTCA) and automated microscopy (Cell-IQ) compared to formazan bioreduction (MTS assay). For validation of the label-free systems different concentrations of ethanol and of amine (AMI) polystyrene NPs were used. CNTs were evaluated in various cell lines, but only endothelial EAhy926 cells and L929 and V79 fibroblasts could be evaluated in all systems. Polystyrene particles obtained similar results in all assays. All systems identified thin (<8 nm) CNTs as more cytotoxic than thick (>20 nm) CNTs, but detection by xCELLigence system was less sensitive to CNT-induced cytotoxicity. Despite advantages, such as continuous monitoring and more detailed analysis of cytotoxic effects, label-free techniques cannot be generally recommended for cytotoxicity screening of NPs.

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“…Culture. The 2BS cell line isolated from human fetal lung fibroblasts was originally established by the National Institute of Biological Products (Beijing, China) and has been well characterized and widely used as a cellular senescence model [23][24][25]. Cells are considered to be young at earlier than 30 population doubling (PD) and replicative senescent around 55PD or later.…”

Section: Cellmentioning

confidence: 99%

Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a miR-22/SIRT-1 Pathway

Mao

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Calorie restriction (CR) is a nongenetic intervention with a robust effect on delaying aging in mammals and other organisms. A mild stimulation on mitochondrial biogenesis induced by CR seems to be an important action mode for its benefits. Here, we reported that a component isolated from Rhodiola rosea L., salidroside, delays replicative senescence in human fibroblasts, which is related to its stimulation on mitochondrial biogenesis by activating SIRT1 partly resulted from inhibition on miR-22. Salidroside increased the mitochondrial mass that accompanied an increment of the key regulators of mitochondrial biogenesis including PGC-1α, NRF-1, and TFAM and reversed the mitochondrial dysfunction in presenescent 50PD cells, showing a comparable effect to that of resveratrol. SIRT1 is involved in the inducement of mitochondrial biogenesis by salidroside. The declined expression of SIRT1 in 50PD cells compared with the young 30PD cells was prevented upon salidroside treatment. In addition, pretreatment of EX-527, a selective SIRT1 inhibitor, could block the increased mitochondrial mass and decreased ROS production induced by salidroside in 50PD cells, resulting in an accelerated cellular senescence. We further found that salidroside reversed the elevated miR-22 expression in presenescent cells according to a miRNA array analysis and a subsequent qPCR validation. Enforced miR-22 expression by using a Pre-miR-22 lentiviral construct induced the young fibroblasts (30PD) into a senescence state, accompanied with increased senescence-related molecules including p53, p21, p16, and decreased SIRT1 expression, a known target of miR-22. However, salidroside could partly impede the senescence progression induced by lenti-Pre-miR-22. Taken together, our data suggest that salidroside delays replicative senescence by stimulating mitochondrial biogenesis partly through a miR22/SIRT1 pathway, which enriches our current knowledge of a salidroside-mediated postpone senility effect and provides a new perspective on the antidecrepitude function of this naturally occurring compound in animals and humans.

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Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose

Cited by 55 publications

References 31 publications

Improvement of Huangqi Decoction on Endothelial Dysfunction in 5/6 Nephrectomized Rats

Improvement of Huangqi Decoction on Endothelial Dysfunction in 5/6 Nephrectomized Rats

Suitability of Cell-Based Label-Free Detection for Cytotoxicity Screening of Carbon Nanotubes

Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a miR-22/SIRT-1 Pathway

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