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혈전성 혈소판감소성 자반증으로 발현된 전신홍반루푸스 1예
오명근,유미라,변유미,윤찬영,권세훈,박치영,김상현 朝鮮大學校 附設 醫學硏究所 2007 The Medical Journal of Chosun University Vol.32 No.3
Thrombotic thrombocytopenic purpura (TTP) is a life-threatening syndrome characterized by the classic pentad of clinical features that includes microangiopathic hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever, and renal dysfunction. Early diagnosis and utilization of plasmapheresis can improve the survival rates of patients with TTP. TTP rarely may be seen in association with autoimmune disease such as systemic lupus erythematous (SLE). We report here a 42-year-old female who was presented with severe digital gangrenes, microangiopathic hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever, and renal dysfunction. Her condition responded to combined therapy with high dose steroid, immunosuppressants, and plasmapheresis therapy.
당뇨 쥐에서 리치로부터 분리된 저분자 폴리페놀인 Oligonol의 NADPH Oxidase 의존형 활성산소종 생산을 통한 세포사 및 췌장보호 효과
Chan Hum Park,Takako Yokozawa,Eun Suk Lee,Young Ock Kim,Sang Won Lee,Yu Su Shin 한국약용작물학회 2017 한국약용작물학술대회 발표집 Vol.2017 No.05
Background : We have previously reported that Oligonol, a low-molecular polyphenol derived from lychee fruit, has protective effect on the liver and kidney of diabetic animal model. In this study, we examined whether Oligonol has any beneficial effects on pancreas of diabetic rats. Methods and Results : Oligonol was orally administered at a dose of 10 and 20 mg/kg body weight for 10 days to STZ-induced diabetic rats, and the effects were compared with those of vehicle-treated diabetic control and non-diabetic control rats. The administration of Oligonol reduced hyperglycemia in diabetic rats through an improvement of serum and pancreatic insulin levels. The increased reactive oxygen species levels in pancreas of diabetic control rats was attenuated by the Oligonol administration through inhibiting the expression of NADPH oxidase-related proteins. The enhanced expression of pro-apoptotic proteins in pancreas of diabetic control rats was significantly reduced by Oligonol administration through down-regulation of phosphor-c-Jun N-terminal kinases protein in pancreas. Furthermore, the expressions of cell proliferation-related protein were also augmented in Oligonol treated-diabetic rats. However, Oligonol treatment led to improved histological changes in the pancreas. Conclusion : These pancreatoprotective effects of Oligonol were achieved through attenuation of oxidative stress and its sensitive protein expression associated with apoptosis and cell proliferation in diabetic rats.
시스플라틴으로 유발된 신장독성 마우스에서 잇꽃씨 폴리페놀의 신장 보호 효과
Chan Hum Park,Eun Suk Lee,Chun Geun Park,Takako Yokozawa,Yu Su Shin 한국약용작물학회 2016 한국약용작물학술대회 발표집 Vol.2016 No.10
Background : In this study, we investigated the renoprotective effects of serotonin and its derivatives, on the renal function and expression of inflammation and apoptosis in cisplatin-induced nephrotoxicity mice. Methods and Results : Serotonin and its derivatives were orally administered at a dose of 7.5 mg/kg body weight for 5 days before the intraperitoneal injection of cisplatin 20 mg/kg body weight, and the effects were compared with those of vehicle-treated nephrotoxicity control and normal groups. In the serum and kidney, renal function parameters, reactive oxygen species and expression of protein related to pro-oxidant, antioxidant, inflammation and apoptosis were examined. As a result, serotonin and its derivatives administrations to nephrotoxicity mice lowered serum BUN and creatinine concentrations. These results were derived, at least in part, from attenuation the expression of antioxidant enzymes-related proteins, SOD and GPx. In the cisplatin-induced renal condition, augmented p-p38, p-ERK and p-JNK (mitogen-activated protein kinase pathway) were reduced with a increase in antioxidant enzymes on serotonin and its derivatives treatment. Moreover, in the serotonin and its derivatives-treated groups, NF- κB-induced inflammatory factors and apoptotic protein expressions were regulated in the kidney. Conclusion : The present study indicates that serotonin and its derivatives exerts a renoprotective effect against cisplatin-induced nephrotoxicity through the recovery of kidney function deterioration and attenuation of renal inflammation and apoptosis by regulating oxidative stress condition.
NF-κB signaling is key in the wound healing processes of silk fibroin
Park, Ye Ri,Sultan, Md. Tipu,Park, Hyun Jung,Lee, Jung Min,Ju, Hyung Woo,Lee, Ok Joo,Lee, Dong Jin,Kaplan, David L.,Park, Chan Hum Elsevier Science B.V. Amsterdam 2018 ACTA BIOMATERIALIA Vol. No.
<P><B>Abstract</B></P> <P>Silk fibroin (SF) is a well-studied biomaterial for tissue engineering applications including wound healing. However, the signaling mechanisms underlying the impact of SF on this phenomenon have not been determined. In this study, through microarray analysis, regulatory genes of NF-ĸB signaling were activated in SF-treated NIH3T3 cells along with other genes. Immunoblot analysis confirmed the activation of the NF-ĸB signaling pathway as SF induced protein expression levels of IKKα, IKKβ, p65, and the degradation of IκBα. The treatment of NIH3T3 cells with SF also increased the expression of cyclin D1, vimentin, fibronectin, and vascular endothelial growth factor (VEGF). The expression of these factors by SF treatment was abrogated when NF-ĸB was inhibited by a pharmacological inhibitor Bay 11-7082. Knockdown of NF-ĸB using siRNA of IKKα and IKKβ also inhibited the SF-induced wound healing response of the NIH3T3 cells in a wound scratch assay. Collectively, these results indicated that SF-induced wound healing through the canonical NF-κB signaling pathway via regulation of the expression of cyclin D1, vimentin, fibronectin, and VEGF by NIH3T3 cells. Using an <I>in vivo</I> study with a partial-thickness excision wound in rats we demonstrated that SF-induced wound healing via NF-κB regulated proteins including cyclin D1, fibronectin, and VEGF. The <I>in vitro</I> and <I>in vivo</I> data suggested that SF induced wound healing via modulation of NF-ĸB signaling regulated proteins.</P> <P><B>Statement of Significance</B></P> <P>Silk fibroin has been effectively used as a dressing for wound treatment for more than a century. However, mechanistic insight into the basis for wound healing via silk fibroin has not been elucidated. Here we report a key mechanism involved in silk fibroin induced wound healing both <I>in vitro</I> and <I>in vivo.</I> Using genetic- and protein-level analyses, NF-κB signaling was found to regulate silk fibroin-induced wound healing by modulating target proteins. Thus, the NF-κB signaling pathway may be utilized as a therapeutic target during the formulation of silk fibroin-based biomaterials for wound healing and tissue engineering.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>