Heme oxygenase-1 induction by (S)-enantiomer of YS-51 (YS-51S), a synthetic isoquinoline alkaloid, inhibits nitric oxide production and nuclear factor-κB translocation in ROS 17/2.8 cells activated with inflammatory stimulants

Chaea, Han-Jung; Kim, Hyung‐Ryong; Kang, Young Jin; Hyun, Kwang Chul; Kim, Hye Jung; Seo, Han Geuk; Lee, Jae Heun; Yun‐Choi, Hye Sook; Chang, Ki Churl

doi:10.1016/j.intimp.2007.07.023

Cited by 19 publications

(12 citation statements)

References 39 publications

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“…However, it should be noted that YS-51 has antioxidant action by induction of Mn-SOD mRNA (Seo et al, 2004) and HO-1 activation effect in endothelial cells (Heo et al, 2007;Chaea et al, 2007). Interestingly, hepatic MnSOD activity is suppressed in male rodent and human NAFLD (Krautbauer et al, 2013), and Sirt1 induces MnSOD via stimulation of Peroxisome proliferator-activated receptor-γ-co-activator-1 (PGC-1 a key regulator of energy metabolism (Pfluger et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Previously, we reported that a series of synthetic tetrahydroisoquinoline alkaloids (THIs) including (S)YS-51 ( Fig. 1) showed beneficial effects in septic mice and in lipopolysaccharide (LPS)-activated RAW264.7 cells by reducing HMGB1 secretion (Chaea et al, 2007;Heo et al, 2007). In particular, (S)-enantiomer was superior to the corresponding (R)-enantiomer in attenuating disseminated intravascular coagulation and multiple organ failure in LPS-treated mice (Pyo et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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(S)YS-51, a novel isoquinoline alkaloid, attenuates obesity-associated non-alcoholic fatty liver disease in mice by suppressing lipogenesis, inflammation and coagulation

Park

Kim

et al. 2016

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

(S)YS-51, a novel isoquinoline alkaloid, attenuates obesity-associated non-alcoholic fatty liver disease in mice by suppressing lipogenesis, inflammation and coagulation

Park

Kim

et al. 2016

European Journal of Pharmacology

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“…28 The scavenging efficiencies of nanofullerol against superoxide anions, hydroxyl radicals, and NO were further determined by the pyrogallol autoxidation, 29 Fenton-type reaction, 30 and Griess reaction. 31 Superoxide dismutase (SOD) or mannitol was used as a control for the scavenger of superoxide anions or hydroxyl radicals. The production of NO was detected by a commercial Griess reagent system kit (Promega, Fitchburg, WI, USA) using the protocol attached.…”

Section: Materials and Methods Characterization And Measurement Of Aqmentioning

confidence: 99%

Antioxidative nanofullerol prevents intervertebral disk degeneration

Yang¹,

Jin²,

Lu³

et al. 2014

IJN

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Compelling evidence suggests that reactive oxygen species (ROS) play a pivotal role in disk degeneration. Fullerol nanoparticles prepared in aqueous solution have been demonstrated to have outstanding ability to scavenge ROS. In this report, in vitro and in vivo models were used to study the efficacy of fullerol in preventing disk degeneration. For in vitro experiments, a pro-oxidant H 2 O 2 or an inflammatory cytokine interleukin (IL)-1β was employed to induce degenerated phenotypes in human nucleus pulposus cells encapsulated in alginate beads, and fullerol was added in the culture medium. For the animal study, an annulus-puncture model with rabbit was created, and fullerol was injected into disks. It was shown that cytotoxicity and cellular ROS level induced by H 2 O 2 were significantly diminished by fullerol. IL-1β-induced nitric oxide generation in culture medium was suppressed by fullerol as well. Gene-profile and biochemical assays showed that fullerol effectively reversed the matrix degradation caused by either H 2 O 2 or IL-1β. The animal study delineated that intradiskal injection of fullerol prevented disk degeneration, increasing water and proteoglycan content and inhibiting ectopic bone formation. These results suggest that antioxidative fullerol may have a potential therapeutic application for disk degeneration.

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“…HO-1 knockout mice and HO-1 deficiency in human increased the inflammatory and oxidative stress, as manifested by extensive inflammation in the liver and kidney (Poss and Tonegawa, 1997). Recent reports indicate that HO-1 is expressed in bone cells and may be involved in the regulation of bone homeostasis (Rawlinson et al, 1998;Zwerina et al, 2005;Chae et al, 2006;Chaea et al, 2007).…”

mentioning

confidence: 99%

“…It is also reported that HO-1 is induced in osteoblasts in weight-bearing bone of the rat by mechanical loading, indicating that it may participate the metabolism of osteoblasts (Rawlinson et al, 1998). HO-1 inhibits osteoblastic apoptosis induced by TNF-a via generating carbon monoxide (Chae et al, 2006) and HO-1 also downregulates the production of cytokines by osteoblast (Chaea et al, 2007). However, the effects of HO-1 on osteoblastic differentiation are still not fully clarified.…”

mentioning

confidence: 99%

Upregulation of heme oxygenase‐1 inhibits the maturation and mineralization of osteoblasts

Lin

Tang

Hung

et al. 2009

Journal Cellular Physiology

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Heme-oxygenase-1 (HO-1), an important enzyme involved in vascular disease, transplantation, and inflammation, catalyzes the degradation of heme into carbon monoxide and biliverdin. It has been reported that overexpression of HO-1 inhibits osteoclastogenesis. However, the effect of HO-1 on osteoblast differentiation is still not clear. We here used adenoviral vector expressing recombinant human HO-1 and HO-1 inducer hemin to study the effects of HO-1 in primary cultured osteoblasts. The results showed that induction of HO-1 inhibited the maturation of osteoblasts including mineralized bone nodule formation, alkaline phosphatase activity and decreased mRNA expression of several differentiation markers such as alkaline phosphatase, osteocalcin, and RUNX2. Furthermore, downstream products of HO-1, bilirubin, carbon monoxide, and iron, are involved in the inhibitory action of HO-1. HO-1 can be induced by H(2)O(2), lipopolysaccharide and inflammatory cytokines such as TNF-alpha and IL-1beta in osteoblasts and also in STZ-induced diabetic mice. In addition, endogenous PPARgamma ligand, 15-deoxy-Delta(12,14)-prostaglandin-J2 (15d-PGJ2) markedly increased both mRNA and protein levels of HO-1 in osteoblasts via PI3K-Akt and MAPK pathways. Blockade of HO activity by ZnPP IX antagonized the inhibitory action on osteocalcin expression by hemin and 15d-PGJ2. Our results indicate that upregulation of HO-1 inhibits the maturation of osteoblasts and HO-1 may be involved in oxidative- or inflammation-induced bone loss.

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Heme oxygenase-1 induction by (S)-enantiomer of YS-51 (YS-51S), a synthetic isoquinoline alkaloid, inhibits nitric oxide production and nuclear factor-κB translocation in ROS 17/2.8 cells activated with inflammatory stimulants

Cited by 19 publications

References 39 publications

(S)YS-51, a novel isoquinoline alkaloid, attenuates obesity-associated non-alcoholic fatty liver disease in mice by suppressing lipogenesis, inflammation and coagulation

(S)YS-51, a novel isoquinoline alkaloid, attenuates obesity-associated non-alcoholic fatty liver disease in mice by suppressing lipogenesis, inflammation and coagulation

Antioxidative nanofullerol prevents intervertebral disk degeneration

Upregulation of heme oxygenase‐1 inhibits the maturation and mineralization of osteoblasts

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