The inhibitory activities of the Cordyceps pruinosa butanol fraction (Cp-BF) were investigated by determining inflammatory responses of lipopolysaccharide (LPS)-treated RAW264.7 macrophage cells and by evaluating HCl/ethanol (EtOH)-triggered gastric ulcers in mice. The molecular mechanisms of the inhibitory effects of Cp-BF were investigated by identifying target enzymes using biochemical and molecular biological approaches. Cp-BF strongly inhibited the production of NO and TNF-α, release of reactive oxygen species (ROS), phagocytic uptake of FITC-dextran, and mRNA expression levels of interleukin (IL)-6, inducible NO synthase (iNOS), and tumour necrosis factor-alpha (TNF)-α in activated RAW264.7 cells. Cp-BF also strongly down regulated the NF-κB pathway by suppressing IKKβ according to luciferase reporter assays and immunoblot analysis. Furthermore, Cp-BF blocked both increased levels of NF-κB-mediated luciferase activities and phosphorylation of p65/p50 observed by IKKβ overexpression. Finally, orally administered Cp-BF was found to attenuate gastric ulcer and block the phosphorylation of IκBα induced by HCl/EtOH. Therefore, these results suggest that the anti-inflammatory activity of Cp-BF may be mediated by suppression of IKKα and its downstream NF-κB activation. Since our group has established the mass cultivation conditions by developing culture conditions for Cordyceps pruinosa, the information presented in this study may be useful for developing new anti-inflammatory agents.

4-isopropyl-2,6-bis(1-phenylethyl)aniline 1 (KTH13-AD1) is a metabolite of Cordyceps bassiana that has been traditionally used to treat various inflammatory disease. Even though it has the magnificent pharmaceutical potential, there was not much understanding on its anti-inflammatory actions. Therefore, this study was aimed to determine the anti-inflammatory effects of KTH13-AD1. We found that KTH13-AD1 suppressed nitric oxide (NO) and reactive oxygen species (ROS) production in lipopolysaccharide (LPS)- or sodium nitroprusside (SNP)-treated macrophages (RAW264.7 cells). Similarly, mRNA expression of inducible NO synthase (iNOS) and tumor necrosis factor-a (TNF-a) analyzed by RT-PCR and real-time PCR was also reduced by this compound. Interestingly, KTH13-AD1 also strongly diminished the levels of NF-kB-mediated luciferase activities and nuclear translocated NF-kB family proteins. In agreement with these, KTH13-AD1 suppressed the upstream signaling pathway for NF-kB activation including IkBa, IKKa/b, AKT, p85/PI3K and Src in time- and dose-dependent manners. Therefore, these results strongly suggest that KTH13-AD1 has a strong anti-inflammatory activity via suppression of the NF-kB signaling pathway.

In this study, we aimed to examine the cellular and molecular mechanisms of KTH-13 (4-isopropyl-2,6-bis(1-phenylethyl)phenol) which is derived from Cordyceps staphylindaecola in the cancer cells survival. The apoptotic effect of KTH-13 on various cancer cells, such as C6 glioma, MDA-MB-231 breast cancer, and A549 cells, was determined by MTT assay, and result showed that KTH-13 (0-100mM) dramatically inhibited the cancer cell survival. IC50 of KTH13 were 60.549, 53.512, >100, in C6, MDA-MB-231, and A549, respectively. DNA fragmentation result revealed that MDA-MB-231 cells treated with KTH-13 100mM undergoes apoptosis. To understand the action mechanism of KTH-13, the effect of KTH-13 on caspase which is key regulator of apoptosis was verified. The amount of cleaved capspase-3 and 7, executioner caspases, was increased by KTH-13 treatment, at time dependent (capspase-3 case) and dose dependent manner (caspase-7 case). And the cleavage of caspase-9 which is initiator caspase was also elevated in KTH-13 treated MDA-MB-231 cells showing time dependent manner. However, caspase-8 was not regulated by KTH-13, indicating KTH-13 specifically targets caspase-9 signal. As caspase-9 is closely associated with intrinsic pathway, the involvement of bcl-2 family was identified. Bax, pro-apoptotic molecule, was up-regulated whereas Bcl-2, anti-apoptotic protein, was down-regulated. And the Bax/Bcl-2 ratio was increased about 10 times. Then, the survival signal was also observed. The phosphorylation of Akt and p85 was diminished by KTH-13 treatment at 2,4,6 and 8 hour. Collectively, results suggest that KTH-13 induces cancer cells apoptosis via caspase3, 7, 8 and Bcl-2 family signaling pathway. And the Akt and p85 is also involved in KTH-13 action mechanism.

본 연구는 microfiltration (MF) 적용을 위한 PVdF/GO 하이브리드 나노섬유막(FG) 제조에 관한 것이다. 지지체인 PVdF (polyvinylidene difluoride) 나노섬유막은 N,N-Dimethylacetamide (DMAc)와 아세톤에 PVdF를 녹여 방사용액 제조 후 전기방사법을 이용하여 제조하였다. 본 연구에서 사용된 GO (grapheme oxide) sheets는 Hummer’s 방법에 따라 제조되었으며, PVdF 나노섬유 지지체 위에 에탄올에 분산시킨 GO용액을 분사함으로써, 최종적으로 PVdF/GO 하이브리드 나노섬유막(FG)을 제조하였다. FG막은 SEM, Raman, 접촉각, 기공특성분석장치(Porometer), 만능인장시험기(UTM)를 사용하여 조사하였고, 수투과도 분석은 제작된 셀(Dead-End Cell)을 이용하여 측정하였다. 접촉각 측정 결과로부터 제조된 FG막의 표면이 친수성으로 개질되었음을 확인할 수 있었으며, 수투과도값은 PVdF막에 비해 약 2.5배 향상된 것을 확인할 수 있었다.