The main active components of Curcuma zedoaria reduces collagen deposition in human lung fibroblast via autophagy.

Disordered collagen production by fibroblasts in response to tissue injury contributes to pulmonary fibrosis (PF). Therefore, elimination of collagen deposition has becoming a potential target in PF treatment which despite standard anti-fibrosis regiment still remains challenge. Curcumin and curcumol are regarded as the main active components extraction from the rhizomes of Curcuma zedoaria, which is widely used for inhibition the proliferation of multiple cells. However, the molecular basis for the function of curcumin and curcumol in limiting fibrogenesis still unknown. In this study, we have investigated the effects of curcumin and curcumol in the fibroblast overproliferation model human lung fibroblast (HLF) inducing by TGF-ß1. The growth-inhibitory effects of the components wasn't observed from 8 to 64 µg/ml. Administration of curcumin or curcumol significantly diminished the level of hydroxyproline hydroxyproline and α-smooth muscle actin (α-SMA), also the collagen Ⅰ (Col-Ⅰ) and collagen Ⅲ (Col-Ⅲ) deposition were reduced in the HLF. Furthermore, related to the collagen synthesis proteins including N-terminal pro-peptide for Type Ⅰ collagen (PⅠNP), N-terminal pro-peptide for Type Ⅲ collagen (PⅢNP) and prolyl-hydroxylase (PHD) were degraded gracefully at dose-dependent manner. Autophagy as the scavenger was crippled in TGF-ß1-fibroblast overproliferation HLF, conversely the increased autophagosomes have been spotted in cytoplasm under transmission electron microscope which is consistent with up-regulation of Beclin1 and ATG7 after treatment with curcumin or curcumol in this study. Additionally, blocking autophagy by inhibitor chloroquine (CQ) caused collagen deposition, providing further evidence regard to autophagy activation capacity of curcumin and curcumol. Our findings provide a detailed understanding that the function of curcumin and curcumol on decreasing collagen deposition mediating by autophagy mechanism, which may also inspire the further research on PF at different perspectives.

The current progress in the mechanism of insulin malfunction in central nervous system leading to the spo-radic type of Alzheimer's disease and its applications / 医学研究生学报

Alzheimer's disease is the most common disease which causes dementia in senior citizens. It is a neurodegenerative disease which is characterized by the degradation of the neurons and synapses in the brain. Usually,the irreversible and progressive neuron loss particular in the regions of cortex and hippocampus,the plaques of the accumulation of amyloidosis outside the cells,as well as the neurofibrillary tangles which is made by the hyperphosphorylation of Tau microtubule proteins can be seen in the lesion loca-tion of the patients. The Insulin malfunction in the central nervous system is now regarded as an important pathogenesis of Alzheimer's disease. This review focuses on the development of the knowledge of the mechanism of the malfunction of insulin in the central nervous system leading to the sporadic type of Alzheimer's disease and its applications,aiming to provide a reference in the study of Alzheimer 's disease.