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靈芝水萃液於肉雞發炎模式下對生長性能、腸道型態及盲腸菌相之影響

為了解決cinnamon.official dc的問題，作者莊凱博 這樣論述：

靈芝(Ganoderma lucidum)在過去亞洲地區的傳統文化中就已經被當中藥材廣泛使用在治療或是預防疾病的發生，由於靈芝中的多醣體已被證實具有調節免疫力、抗發炎、抗氧化、抗癌和抗菌等功能，因此本試驗將探討靈芝水萃液作為肉雞抗發炎的飼料添加物之功效。本研究分為三個試驗，試驗一目的為測定靈芝的體外抗菌效果及生物活性成分的定量，試驗二是使用葡聚醣硫酸鈉(dextran sulfate sodium, DSS)作為肉雞促發炎藥物並測試靈芝水萃液對生長性能、腸道型態、抗發炎效果及腸道菌相的影響，試驗三使用脂多醣(lipopolysaccharide, LPS)誘導肉雞發炎並觀察靈芝水萃液對生長性

能、腸道型態、抗發炎效果及腸道菌相的功能。試驗結果顯示，靈芝水對金黃色葡萄球菌及大腸桿菌具有抑菌效果，此外，在兩種攻毒模式中靈芝水萃液都無法改善其生長性能，但在腸道的發炎基因(COX2、iNOS、IL-1β和IL-6) mRNA表現量皆有抑制的效果；在DSS攻毒的試驗中靈芝無法提高小腸的絨毛長度，但在LPS試驗中靈芝水萃液的高低劑量處理和對照組相比都顯著提高空腸和迴腸的絨毛長度；試驗二的腸道菌相豐富度會因為給予靈芝水萃液而顯著提高，並且抑制了變形菌門的比例，試驗三的結果則是可以發現給予高劑量靈芝水萃液處理會使alpha diversity中的simpson和shannon下降，腸道內乳酸桿菌的

數量相對上升，原本因為LPS攻毒而下降的糞桿菌也恢復成和對照組一樣的水平。綜合上述，靈芝水萃液無論是在DSS或是LPS攻毒皆具有抑制發炎反應的效果，並促進腸道內有益菌的含量，且幫助腸道菌群穩定，在LPS試驗中也能提高絨毛長度增加吸收面積，因此靈芝水萃液具有作為抗發炎飼料添加物的潛力。

肝癌細胞線粒體在ROS生成下HSP60介導並調控MAPK信號傳遞的分子機制

為了解決cinnamon.official dc的問題，作者JayaPrakash Mandal 這樣論述：

Our previous studies showed that mitogen-activated protein kinases (MAPKs) are activated by the interaction of protein kinase C (PKC) and reactive oxygen species (ROS) for hepatocellular carcinoma (HCC) progression. However, the relevant mechanisms remained to be clarified in more detail. In this s

tudy, we used two hepatoma cell lines HepG2 and HCC340 as models to investigate the comprehensive ROS-PKC signaling triggered by tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Since mitochondria-derived reactive oxygen species (mtROS) signaling is well known to be involved in tumor prog

ression, we examined whether TPA triggers the generation of mtROS that can crosstalk with PKC. By mtROS assay, TPA maximally induced mtROS generation at 10 min, which could be prevented by the mitochondria-specific scavenger of mtROS, MitoTEMPO. By western blot, we observed TPA induced transient pho

sphorylation of ERK/JNK and expression of transcriptional factors c-jun/c-fos. Using inhibitors of PKC isozymes and mitoTEMPO, the signal pathway was proved to be transmitted in mtROS/PCK-dependent manner. By BIAM-labeling coupled with LC-MS/MS, heat shock protein 60 (HSP60) was identified as the m

ajor oxidative target. Moreover, suppression of HSP60 by HSP60shRNA, HSP60 inhibitor mizoribine, and expression of dominant-negative HSP60 Cys-mutant prevented TPA-induced phosphorylation of MAPKs and expression of c-jun. In the mechanistic study, for oxidation of HSP60 leading to MAPK activation, w

e found Raf kinase inhibitor protein (RKIP), a negative regulator of MAPK and well-known metastatic suppressor, was involved. Using immunoprecipitation (IP)/Western blot analysis, we found TPA induced the dissociation RKIP from HSP60 within 30 min in both HCCs which can be attenuated by inhibitor of

PKC delta, mtROS scavenger and HSP60 Cys-mutant. At the same time, translocation of HSP60 coupled with MAPK from mitochondria to cytosol was observed. These were closely associated with the robust phosphorylation of MAPKs in the cytosol. By transwell migration assay and cell cycle analysis, TPA ind

uced G1 cell cycle arrest and cell migration, respectively, two dichotomous phenotypical changes of HCCs. Such phenotypes were prevented by the inhibitor of mtROS and knockdown of PKC and HSP60. Several migratory genes such as MMP1/3 (matrix metalloproteinase), LAMC2 (laminin????2), Hic-5 (hydrogen

peroxide inducible clone-5), and a miR-6134, targeting CCNE1 (cyclin E1) were upregulated by TPA. In addition, transcriptional system AP-1 (c-jun/c-fos) regulated TPA-induced migratory genes and miR-6134.In conclusion, we established TPA-induced PKC-mtROS-HSP60 (RKIP)-MAPK-(AP-1) signal axis requi

red for regulating gene expressions triggering dichotomous phenotype in HCCs. Several key players in this pathway such as PKCδ, RKIP, and HSP60 are promising candidates for targeted therapy to prevent HCC progression.