<i>Ginkgo biloba</i>extract attenuates oxLDL-induced oxidative functional damages in endothelial cells

Ou, Hsiu‐Chung; Lee, Wen‐Jane; Lee, I-Te; Chiu, Tsan-Hung; Tsai, Kun Ling; Lin, Chia Yi; Sheu, Wayne Huey‐Herng

doi:10.1152/japplphysiol.91415.2008

Cited by 65 publications

(53 citation statements)

References 56 publications

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“…The expression of Bcl-2 was decreased in pEGFP-C1 transfected 293T cells stimulated by oxLDL and was decreased further in pEGFP-C1-SR-AI transfected 293T cells. These results might be due to an increased SR-AI-mediated uptake of oxLDL and are consistent with the observation that oxLDL disturbs the balance of Bcl-2 family proteins in endothelial cells [23]. It has been reported previously for vascular SMCs and for human THP-1 monocyte-derived macrophages that oxLDL decreased Bcl-2 expression and increased Bax expression [24,25].…”

Section: Discussionsupporting

confidence: 91%

Effect of overexpression of human SR-AI on oxLDL uptake and apoptosis in 293T cells

Yang

Chen

Yongqing

et al. 2011

International Immunopharmacology

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Section: Discussionsupporting

confidence: 91%

Effect of overexpression of human SR-AI on oxLDL uptake and apoptosis in 293T cells

Yang

Chen

Yongqing

et al. 2011

International Immunopharmacology

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“…ROS generation is often responsible for the mitochondria-mediated signaling pathway of apoptosis (27). In the present study, we found that the ROS generation was the earliest apoptotic signal, usually occurring within 15 min after the addition of Ang II.…”

Section: Discussionsupporting

confidence: 58%

Role of LOX-1 in Ang II-induced oxidative functional damage in renal tubular epithelial cells

Shi-wei²,

Xie³

et al. 2010

Int J Mol Med

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Abstract. The lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), plays an important role in angiotension II (Ang II)-induced hypertensive renal injury associated with pro-inflammatory responses, tubular functional damage and cellular apotosis. In this study, we report on the role of LOX-1 in Ang II-induced oxidative functional damage and underlying signaling in human renal proximal tubular epithelial cells (HRPTEpiCs). The exposure to Ang II enhanced the expression of the NADPH oxidases (the p22phox, p47phox and Nox4 subunits), LOX-1 and the adhesion molecule, ICAM-1. It also promoted monocytic U937 cell adherences to HRPTEpiCs, increased reactive oxygen species formation and stimulated apotosis, which was concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases (MAPK). Furthermore, the Ang II treatment disturbed the balance of the Bcl-2 family proteins, destabilized mitochondrial membrane potential, and subsequently triggered the release of cytochrome c into the cytosol, causing the activation of caspase-3. The NADPH oxidase inhibitors and LOX-1 small interfering RNA markedly ameliorated these detrimental effects by reducing LOX-1 expression and MAPK activation. The p38 and p44/42MAPK inhibitors also inhibited the Ang II-induced functional damage without affecting LOX-1 expression in the HRPTEpiCs. These observations suggest that LOX-1 mediates Ang II-induced renal tubular epithelial dysfunction. In addition, MAPK pathway activation occurs downstream of the Ang II/reactive oxygen species/ LOX-1 cascade.

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“…It not only reduced the deposition of calcium, but also inhibited osteogenic transdifferentiation, which are consistent with experimental animal studies and with clinical studies linking EGb 761 to beneficial effects on VC. 14,19,[29][30][31] However, the detailed mechanism by which EGb 761 may influence this process is unclear. More research is required to observe the EGb 761 in patients with renal failure and to confirm a possible protective effect of EGb 761 against VC.…”

Section: Discussionmentioning

confidence: 99%

Effects of Gingko biloba extract (EGb 761) on vascular smooth muscle cell calcification induced by β-glycerophosphate

Tian

2016

Renal Failure

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Objective To investigate the effects of Gingko biloba extract (EGb 761) on calcification induced by b-glycerophosphate in rat aortic vascular smooth muscle cells. Methods Rat aortic vascular smooth muscle cells were cultured with various concentrations of EGb 761 and b-glycerophosphate for 7 days. Calcium content in the cells, alkaline phosphatase activity, cell protein content, NF-kB activation, and reactive oxygen species production were assayed, respectively. Results The calcium depositions of vascular smooth muscle cells of the b-glycerophosphate group were significantly higher than those of the control group (p50.01), and were inhibited by EGb 761 in a concentration-dependent manner (p50.05). Data showed b-glycerophosphate induced the enhanced expression of alkaline phosphatase, up-regulated the NF-kB activity and increased reactive oxygen species production of vascular smooth muscle cells while these decreased when administrated with EGb 761(p50.05). Conclusions EGb 761 significantly reduced deposition of calcium induced by b-glycerophosphate in rat aortic vascular smooth muscle cells. It not only reduced the deposition of calcium, but also inhibited osteogenic transdifferentiation, which may be associated with decreasing expression of alkaline phosphatase, down-regulating the NF-kB activity, and reducing reactive oxygen species production of vascular smooth muscle cells, and may have the potential to serve as a role for vascular calcification in clinical situations. ARTICLE HISTORY

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Ginkgo bilobaextract attenuates oxLDL-induced oxidative functional damages in endothelial cells

Abstract: Ou HC, Lee WJ, Lee IT, Chiu TH, Tsai KL, Lin CY, Sheu WH. Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells.

Cited by 65 publications

References 56 publications

Effect of overexpression of human SR-AI on oxLDL uptake and apoptosis in 293T cells

Effect of overexpression of human SR-AI on oxLDL uptake and apoptosis in 293T cells

Role of LOX-1 in Ang II-induced oxidative functional damage in renal tubular epithelial cells

Effects of Gingko biloba extract (EGb 761) on vascular smooth muscle cell calcification induced by β-glycerophosphate

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