Guggulsterone attenuates cerulein-induced acute pancreatitis via inhibition of ERK and JNK activation

Kim, Dong-Goo; Bae, Gi‐Sang; Choi, Sun-Bok; Jo, Il‐Joo; Shin, Joon-Yeon; Lee, Sung-Kon; Kim, Myoung-Jin; Kim, Minjun; Jeong, Hyun‐Woo; Lee, Jang Ho; Seo, Sang‐Woo; Choo, Gab-Chul; Seo, Sang-Wan; Song, Ho‐Joon; Park, Sung‐Joo

doi:10.1016/j.intimp.2015.03.030

Cited by 36 publications

(21 citation statements)

References 48 publications

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“…AP was induced by six intraperitoneal (IP) injections of caerulein (50 μg/kg, at 1 h intervals) as described previously 52 . Each experimental group contained five mice.…”

Section: Methodsmentioning

confidence: 99%

NAD+ augmentation ameliorates acute pancreatitis through regulation of inflammasome signalling

Shen¹,

Kim²,

Oh³

et al. 2017

Sci Rep

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Acute pancreatitis (AP) is a complicated disease without specific drug therapy. The cofactor nicotinamide adenine dinucleotide (NAD+) is an important regulator of cellular metabolism and homeostasis. However, it remains unclear whether modulation of NAD+ levels has an impact on caerulein-induced AP. Therefore, in this study, we investigated the effect of increased cellular NAD+ levels on caerulein-induced AP. We demonstrated for the first time that the activities and expression of SIRT1 were suppressed by reduction of intracellular NAD+ levels and the p53-microRNA-34a pathway in caerulein-induced AP. Moreover, we confirmed that the increase of cellular NAD+ by NQO1 enzymatic action using the substrate β-Lapachone suppressed caerulein-induced AP with down-regulating TLR4-mediated inflammasome signalling, and thereby reducing the inflammatory responses and pancreatic cell death. These results suggest that pharmacological stimulation of NQO1 could be a promising therapeutic strategy to protect against pathological tissue damage in AP.

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“…AP was induced by six intraperitoneal (IP) injections of caerulein (50 μg/kg, at 1 h intervals) as described previously 52 . Each experimental group contained five mice.…”

Section: Methodsmentioning

confidence: 99%

NAD+ augmentation ameliorates acute pancreatitis through regulation of inflammasome signalling

Shen¹,

Kim²,

Oh³

et al. 2017

Sci Rep

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“…Evidence showed that GS attenuated pancreatitis via inhibition of JNK activation (Kim et al . ; Tsai et al . ).…”

Section: Resultsmentioning

confidence: 95%

Z‐Guggulsterone attenuates astrocytes‐mediated neuroinflammation after ischemia by inhibiting toll‐like receptor 4 pathway

Liu

Zhang

et al. 2018

Journal of Neurochemistry

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Inflammatory damage plays a pivotal role in ischemic stroke pathogenesis and may represent one of the therapeutic targets. Z-Guggulsterone (Z-GS), an active component derived from myrrh, has been used to treat various diseases. The traditional uses suggest that myrrh is a good candidate for anti-inflammatory damage. This study was to investigate the anti-inflammatory and neuroprotective effects of Z-GS following cerebral ischemic injury, as well as the exact mechanisms behind them. Rat middle cerebral artery occlusion (MCAO) model and in vitro astrocytes oxygen-glucose deprivation (OGD) model were adopted to simulate ischemic stroke. Z-GS (30 or 60 mg/kg) was administered intraperitoneally immediately after reperfusion, while astrocytes were maintained in 30 or 60 μM Z-GS before OGD treatment. The results indicated that Z-GS significantly alleviated neurological deficits, infarct volume and histopathological damage in vivo, and increased the astrocytes viability in vitro. Moreover, the treatment of Z-GS inhibited the astrocytes activation and down-regulated the mRNA levels of pro-inflammatory cytokines. Furthermore, the activated TLR4-NF-κB signaling pathways induced by MCAO or OGD were significantly suppressed by Z-GS treatment, which was achieved via inhibiting the phosphorylation of JNK. Our results demonstrated that Z-GS exerted neuroprotective and anti-inflammatory properties through preventing activation of TLR4-mediated pathway in the activated astrocytes after ischemia injury. Therefore, Z-GS could be considered as a promising candidate for the treatment of ischemic stroke.

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“…They reported that reduction of neutrophil accumulation, depletion of neutrophils, and inhibited infiltrations of macrophages and neutrophils improved systemic events during experimental AP. [18][19][20] Therefore, chemicals that improve neutrophil functions may reduce detrimental systemic effects of AP.…”

Section: Discussionmentioning

confidence: 99%

Effect of N-acetylcysteine on neutrophil functions during experimental acute pancreatitis

Atayoğlu¹,

Gurleyik

Demirel³

et al. 2016

Ulus Travma Acil Cerrahi Derg

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BACKGROUND: Systemic inflammatory responses and extrapancreatic vital organ impairment are mediated by activated neutrophil functions and products, such as oxygen-derived free radicals, in patients with acute pancreatitis (AP). The present study is an examination of effects of an antioxidant, N-acetylcysteine (NAC), on local and systemic histopathological changes and neutrophil functions during AP.

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Guggulsterone attenuates cerulein-induced acute pancreatitis via inhibition of ERK and JNK activation

Cited by 36 publications

References 48 publications

NAD+ augmentation ameliorates acute pancreatitis through regulation of inflammasome signalling

NAD+ augmentation ameliorates acute pancreatitis through regulation of inflammasome signalling

Z‐Guggulsterone attenuates astrocytes‐mediated neuroinflammation after ischemia by inhibiting toll‐like receptor 4 pathway

Effect of N-acetylcysteine on neutrophil functions during experimental acute pancreatitis

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