AIM: To investigate the anti-proliferative and apoptotic effects of Chaga mushroom (Inonotus obliquus) water extract on human hepatoma cell lines,HepG2 and Hep3B cells. METHODS: The cytotoxicity of Chaga extract was s...AIM: To investigate the anti-proliferative and apoptotic effects of Chaga mushroom (Inonotus obliquus) water extract on human hepatoma cell lines,HepG2 and Hep3B cells. METHODS: The cytotoxicity of Chaga extract was screened by 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT) assay. Morphological observation,flow cytometry analysis,Western blot were employed to elucidate the cytotoxic mechanism of Chaga extract. RESULTS: HepG2 cells were more sensitive to Chaga extract than Hep3B cells,as demonstrated by markedly reduced cell viability. Chaga extract inhibited the cell growth in a dose-dependent manner,which was accompanied with G0/G1-phase arrest and apoptotic cell death. In addition,G0/G1 arrest in the cell cycle was closely associated with down-regulation of p53,pRb,p27,cyclins D1,D2,E,cyclin-dependent kinase (Cdk) 2,Cdk4,and Cdk6 expression. CONCLUSION: Chaga mushroom may provide a new therapeutic option,as a potential anticancer agent,in the treatment of hepatoma.展开更多
AIM： To investigate the effect of selective Cyclooxygenase-2 （COX-2） inhibitor 4-[5-（4-Chloro-phenyl）-3- （trifluoromethyl）- 1H-pyrazol- 1-yl] benzenesulfonamide （SC-236）, on the cholecystokinin （CCK）-octape...AIM： To investigate the effect of selective Cyclooxygenase-2 （COX-2） inhibitor 4-[5-（4-Chloro-phenyl）-3- （trifluoromethyl）- 1H-pyrazol- 1-yl] benzenesulfonamide （SC-236）, on the cholecystokinin （CCK）-octapeptideinduced acute pancreatitis （AP） in rats. METHODS： Wistar rat weighing 240 g to 260 g were divided into three groups. （1） Normal DMSO treated group, （2） SC-236 at 4 mg/kg treated group; SC-236 systemically administered via the intravenous （i.v.） catheter, followed by 75 μg/kg CCK octapeptide subcutaneously three times, after 1, 3 and 5 h. This whole procedure was repeated for 5 d. （3） Dimethyl sulfoxide （DMSO） treated group： an identical protocol was used in this group as in the SC-236 cohort （see 2. above）. Repeated CCK octapeptide treatment resulted in a typical experimentally induced pancreatitis in the Wistar rats. RESULTS： SC-236 improved the severity of CCK- octapeptide-induced AP as measured by laboratory criteria [the pancreatic weight/body weight （p.w/ b.w） ratio, the level of serum amylase and lipase]. The SC-236 treated group showed minimal histologic evidence of pancreatitis and a significant reduction in myeloperoxidase activity. SC-236 also increased heat shock protein （HSP）-60 and HSP72 compared with the DMSO-treated group in the CCK-octapeptide-induced AP and also reduced the pancreatic levels of COX-2. Furthermore, SC-236 reduced proinflammatory cytokine synthesis and inhibited NF-KB activation compared with the DMSO-treated group in the CCK-octapeptide-induced AP. CONCLUSION： Our results suggested that COX-2 plays pivotal role in the development of AP and COX-2 inhibitors may play a beneficial role in preventing AP.展开更多
AIM： To investigate the effect of Garden/a fasm/noides （GJ） on cerulein-induced acute pancreatitis （AP） in mice. METHODS： C57BL/6 mice weighing 18-20 g were divided into three groups. （1） Normal salinetreated ...AIM： To investigate the effect of Garden/a fasm/noides （GJ） on cerulein-induced acute pancreatitis （AP） in mice. METHODS： C57BL/6 mice weighing 18-20 g were divided into three groups. （1） Normal salinetreated 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 anintraperitoneal injection of cerulein （50 μg/kg）, a stable cholecystokinin （CCK） analogue, every hour for a total of 6h 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℃ 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. RESULTS： Treatment with G.1 decreased significantly the severity of pancreatitis and pancreatitis-associated lung injury. Treatment with G.1 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. CONCLUSION： These results suggest that GJ attenuated the severity of AP as well as pancreatitisassociated lung injury.展开更多
基金the Program for the Training of Graduate Students in Regional Innovation which was conducted by the Ministry of Commerce Industry and Energy of the Korean Government
文摘AIM: To investigate the anti-proliferative and apoptotic effects of Chaga mushroom (Inonotus obliquus) water extract on human hepatoma cell lines,HepG2 and Hep3B cells. METHODS: The cytotoxicity of Chaga extract was screened by 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT) assay. Morphological observation,flow cytometry analysis,Western blot were employed to elucidate the cytotoxic mechanism of Chaga extract. RESULTS: HepG2 cells were more sensitive to Chaga extract than Hep3B cells,as demonstrated by markedly reduced cell viability. Chaga extract inhibited the cell growth in a dose-dependent manner,which was accompanied with G0/G1-phase arrest and apoptotic cell death. In addition,G0/G1 arrest in the cell cycle was closely associated with down-regulation of p53,pRb,p27,cyclins D1,D2,E,cyclin-dependent kinase (Cdk) 2,Cdk4,and Cdk6 expression. CONCLUSION: Chaga mushroom may provide a new therapeutic option,as a potential anticancer agent,in the treatment of hepatoma.
基金Supported by the Ministry of Science & Technology/Korea Science & Engineering Foundation through the Vestibuloco-chlear Research Center at Wonkwang University, No. R13-2002- 055-00000-0
文摘AIM： To investigate the effect of selective Cyclooxygenase-2 （COX-2） inhibitor 4-[5-（4-Chloro-phenyl）-3- （trifluoromethyl）- 1H-pyrazol- 1-yl] benzenesulfonamide （SC-236）, on the cholecystokinin （CCK）-octapeptideinduced acute pancreatitis （AP） in rats. METHODS： Wistar rat weighing 240 g to 260 g were divided into three groups. （1） Normal DMSO treated group, （2） SC-236 at 4 mg/kg treated group; SC-236 systemically administered via the intravenous （i.v.） catheter, followed by 75 μg/kg CCK octapeptide subcutaneously three times, after 1, 3 and 5 h. This whole procedure was repeated for 5 d. （3） Dimethyl sulfoxide （DMSO） treated group： an identical protocol was used in this group as in the SC-236 cohort （see 2. above）. Repeated CCK octapeptide treatment resulted in a typical experimentally induced pancreatitis in the Wistar rats. RESULTS： SC-236 improved the severity of CCK- octapeptide-induced AP as measured by laboratory criteria [the pancreatic weight/body weight （p.w/ b.w） ratio, the level of serum amylase and lipase]. The SC-236 treated group showed minimal histologic evidence of pancreatitis and a significant reduction in myeloperoxidase activity. SC-236 also increased heat shock protein （HSP）-60 and HSP72 compared with the DMSO-treated group in the CCK-octapeptide-induced AP and also reduced the pancreatic levels of COX-2. Furthermore, SC-236 reduced proinflammatory cytokine synthesis and inhibited NF-KB activation compared with the DMSO-treated group in the CCK-octapeptide-induced AP. CONCLUSION： Our results suggested that COX-2 plays pivotal role in the development of AP and COX-2 inhibitors may play a beneficial role in preventing AP.
基金The Ministry of Science & Technology (MoST)/Korea Science & Engineering Foundation (KOSEF) through the Vestibulocochlear Research Center (VCRC) at Wonkwang University (R13-2002-055-00000-0)
文摘AIM： To investigate the effect of Garden/a fasm/noides （GJ） on cerulein-induced acute pancreatitis （AP） in mice. METHODS： C57BL/6 mice weighing 18-20 g were divided into three groups. （1） Normal salinetreated 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 anintraperitoneal injection of cerulein （50 μg/kg）, a stable cholecystokinin （CCK） analogue, every hour for a total of 6h 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℃ 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. RESULTS： Treatment with G.1 decreased significantly the severity of pancreatitis and pancreatitis-associated lung injury. Treatment with G.1 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. CONCLUSION： These results suggest that GJ attenuated the severity of AP as well as pancreatitisassociated lung injury.
