-
Gi-Sang Bae,
Min-Sun Kim,
Jinsu Jeong,
Hye-Youn Lee,
Kyoung-Chel Park,
Bon Soon Koo,
Byung-Jin Kim,
Tae-Hyeon Kim,
Seung Ho Lee, Sung-Yeon Hwang,
Yong Kook Shin,
Ho-Joon Song,
Sung-Joo Park
[show abstract]
[hide abstract]
ABSTRACT: Piperine is a phenolic component of black pepper (Piper nigrum) and long pepper (Piper longum), fruits used in traditional Asian medicine. Our previous study showed that piperine inhibits lipopolysaccharide-induced inflammatory responses. In this study, we investigated whether piperine reduces the severity of cerulein-induced acute pancreatitis (AP). Administration of piperine reduced histologic damage and myeloperoxidase (MPO) activity in the pancreas and ameliorated many of the examined laboratory parameters, including the pancreatic weight (PW) to body weight (BW) ratio, as well as serum levels of amylase and lipase and trypsin activity. Furthermore, piperine pretreatment reduced the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 during cerulein-induced AP. In accordance with in vivo results, piperine reduced cell death, amylase and lipase activity, and cytokine production in isolated cerulein-treated pancreatic acinar cells. In addition, piperine inhibited the activation of mitogen-activated protein kinases (MAPKs). These findings suggest that the anti-inflammatory effect of piperine in cerulein-induced AP is mediated by inhibiting the activation of MAPKs. Thus, piperine may have a protective effect against AP.
Biochemical and Biophysical Research Communications 05/2011; 410(3):382-8. · 2.48 Impact Factor
-
Gi-Sang Bae,
Sang-Wan Seo,
Min-Sun Kim,
Kyoung-Chel Park,
Bon Soon Koo,
Won-Seok Jung,
Gil-Hwan Cho,
Hyun Cheol Oh,
Seung-Won Yun,
Jong-Jin Kim,
Sung Gyu Kim, Sung-Yeon Hwang,
Ho-Joon Song,
Sung-Joo Park
[show abstract]
[hide abstract]
ABSTRACT: Nardostachys jatamansi (NJ) has been used in the treatment of inflammatory diseases. However, it is not clear how NJ produces anti-inflammatory effects. In the present study, using an experimental model of lipopolysaccharide (LPS)-induced endotoxin shock, the protective effects and mechanisms of action of NJ were investigated. The water extract of roots of NJ was administrated to mice orally (1, 5, and 10 mg/kg) 1 h after or before LPS challenge. The administration of NJ inhibited LPS-induced endotoxin shock and the production of inflammatory mediators, such as interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-α/β. Murine peritoneal macrophages were used to determine the production of inflammatory mediators. In peritoneal macrophages, NJ also inhibited LPS-induced production of inflammatory mediators, such as IL-1β, IL-6, TNF-α, and IFN-α/β. In addition, NJ reduced the activation of mitogen-activated protein kinases (MAPKs) and the level of expression of interferon regulatory factor (IRF)-1 and IRF-7 mRNA. Furthermore, post-treatment with NJ reduced LPS-induced endotoxin shock and the production of inflammatory mediators. These results suggest that NJ inhibits endotoxin shock by inhibiting the production of IL-1β, IL-6, TNF-α, and IFN-α/β through the inhibition of MAPKs activation and IRF induction.
Journal of Natural Medicines 01/2011; 65(1):63-72. · 1.39 Impact Factor
-
Hee-Je Park,
Hyung-Jin Kim,
Gi-Sang Bae,
Sang-Wan Seo,
Do-Yun Kim,
Won-Seok Jung,
Min-Sun Kim,
Mi-Young Song,
Eun-Kyung Kim,
Kang-Beom Kwon, Sung-Yeon Hwang,
Ho-Joon Song,
Cheung-Seog Park,
Rae-Kil Park,
Myong-Soo Chong,
Sung-Joo Park
[show abstract]
[hide abstract]
ABSTRACT: Glycogen synthase kinase-3 (GSK-3) plays an important role in the regulation of apoptosis. However, the role of GSK-3 in the auditory system remains unknown. Here we examined whether the GSK-3-specific inhibitors, SB 216763 and LiCl, could protect against cisplatin-induced cytotoxicity of auditory cells. GSK-3 was activated by cisplatin treatment of HEI-OC1 cells. SB 216763 or LiCl treatments inhibited cisplatin-induced apoptosis in a dose-dependent manner and activated caspase-9, -8 and -3. In rat primary explants of the organ of Corti, SB 216763 or LiCl treatments completely abrogated the cisplatin-induced destruction of outer hair cell arrays. Administration of SB 216763 or LiCl inhibited cochlear destruction and the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and IL-6 in cisplatin-injected mice. Furthermore, administration of SB 216763 or LiCl reduced the thresholds of the auditory brainstem response (ABR) in cisplatin-injected mice. Collectively, these results suggest that cisplatin-induced ototoxicity might be associated with modulation of GSK-3 activation.
Hearing research 09/2009; 257(1-2):53-62. · 2.18 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Ethanol causes neurotoxicity through formation of reactive oxygen species and activation of mitogen-activated protein kinase (MAPK) pathways. MAPK phosphatase-1 (MKP-1) is one of the phosphatases responsible for dephosphorylation/deactivation of MAPKs. In this report, we examined the potential involvement of MKP-1 in cytoprotective effects of the well-known antioxidant curcumin. In HT22 hippocampal cells, ethanol caused cell death and activation of p38 MAPK and other two kinases. Blockage of p38 MAPK by its inhibitor protected HT22 cells against ethanol-induced toxicity. Curcumin attenuated ethanol-induced cell death, inhibited activation of p38 MAPK, and activated MKP-1. In HT22 cells transiently transfected with small interfering RNA against MKP-1, curcumin failed to inhibit ethanol-induced activation of p38 MAPK and to protect HT22 cells from ethanol-induced toxicity. Our results suggest that curcumin can attenuate ethanol-induced neurotoxicity by activating MKP-1 which acts as the negative regulator of p38 MAPK. This novel pathway may contribute to and explain at least one of the cytoprotective actions of curcumin.
Neuroscience Letters 05/2009; 453(3):186-9. · 2.11 Impact Factor
-
Won-Seok Jung,
Young-Seok Chae,
Do-Yun Kim,
Sang-Wan Seo,
Hee-Je Park,
Gi-Sang Bae,
Tae-Hyeon Kim,
Hyo-Jeong Oh,
Ki-Jung Yun,
Rae-Kil Park,
Jong-Suk Kim,
Eun-Cheol Kim, Sung-Yeon Hwang,
Sung-Joo Park,
Ho-Joon Song
[show abstract]
[hide abstract]
ABSTRACT: To investigate the effect of Gardenia jasminoides (GJ) on cerulein-induced acute pancreatitis (AP) in mice.
C57BL/6 mice weighing 18-20 g were divided into three groups. (1) Normal saline-treated group, (2) treatment with GJ at a dose of 0.1 g/kg, (3) treatment with GJ at a dose of 1 g/kg. GJ was administered orally (n = 6 per group) for 1 wk. Three hours later, the mice were given an intraperitoneal injection of cerulein (50 microg/kg), a stable cholecystokinin (CCK) analogue, every hour for a total of 6 h as described previously. The mice were sacrificed at 6 h after completion of cerulein injections. Blood samples were obtained to determine serum amylase, lipase and cytokine levels. The pancreas was rapidly removed for morphologic examination and scoring. A portion of pancreas was stored at -70 degree and prepared for the measurement of tissue myeloperoxidase (MPO) activity, an indicator of neutrophil sequestration, and for reverse-transcriptase PCR (RT-PCR) and real-time PCR measurements.
Treatment with GJ decreased significantly the severity of pancreatitis and pancreatitis-associated lung injury. Treatment with GJ attenuated the severity of AP compared with saline-treated mice, as shown by reduction in pancreatic edema, neutrophil infiltration, serum amylase and lipase levels, serum cytokine levels, and mRNA expression of multiple inflammatory mediators.
These results suggest that GJ attenuated the severity of AP as well as pancreatitis-associated lung injury.
World Journal of Gastroenterology 11/2008; 14(40):6188-94. · 2.47 Impact Factor
