Hyperoside attenuates hydrogen peroxide-induced L02 cell damage via MAPK-dependent Keap1–Nrf2–ARE signaling pathway

Xing, Haiyan; Liu, Yao; Chen, Jianhong; Sun, Fengjun; Shi, Huiqing; Xia, Peiyuan

doi:10.1016/j.bbrc.2011.06.046

Cited by 64 publications

(36 citation statements)

References 22 publications

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“…40 Unlike in previous reports, the signaling proteins p38 and ERK were protective in our studies, consistent with findings implicating these MAPK pathways in Nrf2-dependent antioxidant production. 41,42 A paradigm has emerged in AKI research in which many growth factors (e.g., epidermal growth factor and IGF) are upregulated after injury and facilitate renal repair. Our studies indicate that TGF-b does not fit this paradigm, probably because its proapoptotic effects on epithelial cells outweigh any beneficial effects in the context of AKI.…”

Section: Discussionmentioning

confidence: 99%

Deleting the TGF-β Receptor Attenuates Acute Proximal Tubule Injury

Gewin

Vadivelu²,

Neelisetty³

et al. 2012

Journal of the American Society of Nephrology

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TGF-b is a profibrotic growth factor in CKD, but its role in modulating the kidney's response to AKI is not well understood. The proximal tubule epithelial cell, which is the main cellular target of AKI, expresses high levels of both TGF-b and its receptors. To determine how TGF-b signaling in this tubular segment affects the response to AKI, we selectively deleted the TGF-b type II receptor in the proximal tubules of mice. This deletion attenuated renal impairment and reduced tubular apoptosis in mercuric chloride-induced injury. In vitro, deficiency of the TGF-b type II receptor protected proximal tubule epithelial cells from hydrogen peroxide-induced apoptosis, which was mediated in part by Smad-dependent signaling. Taken together, these results suggest that TGF-b signaling in the proximal tubule has a detrimental effect on the response to AKI as a result of its proapoptotic effects.

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Section: Discussionmentioning

confidence: 99%

Deleting the TGF-β Receptor Attenuates Acute Proximal Tubule Injury

Gewin

Vadivelu²,

Neelisetty³

et al. 2012

Journal of the American Society of Nephrology

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“…Hyperoside is a flavonol glycoside with variety of biological activities, including antioxidant, anticancer, antihyperglycemic and anti-inflammatory functions (25)(26)(27). However, prior to the current study, hyperoside has demonstrated little antibacterial activity (20,28).…”

Section: Effect Of Hyperoside On P Aeruginosa Biofilm Formationmentioning

confidence: 91%

Hyperoside inhibits biofilm formation of Pseudomonas aeruginosa

Sun

Feng

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Pseudomonas aeruginosa (P. aeruginosa) is a common pathogen in hospital-acquired infection and is readily able to form biofilms. Due to its high antibiotic resistance, traditional antibacterial treatments exert a limited effect on P. aeruginosa biofilm infections. It has been indicated that hyperoside inhibits P. aeruginosa PAO1 (PAO1) biofilm formation without affecting growth. Therefore, the current study examined the biofilm formation and quorum sensing (QS) system of PAO1 in the presence of hyperoside.Confocal laser scanning microscopy analysis demonstrated that hyperoside significantly inhibited biofilm formation. It was also observed that hyperoside inhibited twitching motility in addition to adhesion. Data from reverse transcription-quantitative polymerase chain reaction indicated that hyperoside inhibited the expression of lasR, lasI, rhlR and rhlI genes. These results suggest that the QS-inhibiting effect of hyperoside may lead to a reduction in biofilm formation. However, the precise mechanism of hyperoside on P. aeruginosa pathogenicity remains unclear and requires elucidation in additional studies. IntroductionPseudomonas aeruginosa (P. aeruginosa) is a common pathogen in hospital-acquired infections (1). Due to increasing multidrug resistance, P. aeruginosa infection is an increasingly common cause of mortality and morbidity (2). The mechanisms of antibiotic resistance in P. aeruginosa include the expression of multiple antibiotic modifying enzymes, antibiotic efflux pumps and acquisition of chromosomally or plasmid encoded antibiotic resistance genes. Additionally, chromosomal mutations and lower membrane permeability for the antibiotics also contribute to antibiotic resistance (3).P. aeruginosa is a biofilm-forming pathogen and is difficult to eradicate due to its high antibiotic resistance and the ability of the biofilm to evade the immune system (4-7). Quorum sensing (QS) is a system of stimuli and response correlated to population density. P. aeruginosa uses the QS system to coordinate gene expression according to the density of its local population. Thus, it can coordinate certain behaviors such as biofilm formation, virulence and antibiotic resistance. QS inhibitors (QSIs) are the most well reported alternative therapeutics that can be used to overcome the problem of increasing antibiotic resistance in P. aeruginosa. QSIs target the virulence of the organism and therefore are also termed antipathogenic drugs. The virulence of P. aeruginosa depends on its cell-to-cell communication system, or QS system that uses diffusible signaling molecules that accumulate with increasing cell density and allows P. aeruginosa to trigger coordinated responses and achieve outcomes that would otherwise remain impossible to achieve by individual bacterium (8). Previous studies have demonstrated that traditional treatments for bacteria exert some effect on biofilm infections (9,10). Therefore, the effects of constituents from marine organisms, traditional Chinese herbs and plants (11-13) on biofilm infe...

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“…Hyperoside attenuates H2O2-induced L02 cell damage via MAPK (p38 and ERK)-dependent Keap/Nrf2/ARE signaling pathway (Xing et al, 2011). Thus, whether taraxerolstimulated cytoprotective effect is involved in MAPKdependent Keap/Nrf2/ARE signaling pathway remains elusive.…”

Section: Discussionmentioning

confidence: 99%

Taraxerol protects the human hepatic L02 cells from hydrogen peroxide-induced apoptosis

Yao

Bai

2017

Bangladesh J Pharmacol

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Taraxerol is known to exhibit anti-inflammatory and anti-cancer activity. However, cytoprotective effect of taraxerol on hepatocytes has not been reported. In the present study, we investigated the hepatoprotective effect of taraxerol in the human hepatic L02 cells injured by hydrogen peroxide (H2O2). Taraxerol decreased H2O2-induced cell viability loss and lactate dehydrogenase release. Taraxerol also inhibited H2O2-induced cell apoptosis. Further, taraxerol attenuated H2O2-induced increase in cleaved-caspase-3 and cleaved-PARP. H2O2-activated p38 and JNK were also inhibited by taraxerol. These data suggest that taraxerol could protect the L02 cells against H2O2-induced apoptosis via suppression of p38 and JNK. Taraxerol may be an effective protective agent against oxidative stress-induced liver injury.

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Hyperoside attenuates hydrogen peroxide-induced L02 cell damage via MAPK-dependent Keap1–Nrf2–ARE signaling pathway

Cited by 64 publications

References 22 publications

Deleting the TGF-β Receptor Attenuates Acute Proximal Tubule Injury

Deleting the TGF-β Receptor Attenuates Acute Proximal Tubule Injury

Hyperoside inhibits biofilm formation of Pseudomonas aeruginosa

Taraxerol protects the human hepatic L02 cells from hydrogen peroxide-induced apoptosis

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