// Huijuan Liu 1, 2, * , Qin Tian 1, * , Xiaoyu Ai 1, * , Yuan Qin 1 , Zhanhong Cui 1 , Meng Li 1 , Jiahuan Yang 1 , Denghui Zhai 1 , Yanrong Liu 3 , Shuang Chen 3 , Jing Meng 1 , Tao Sun 1, 3 , Honggang Zhou 1, 3 and Cheng Yang 1, 3 1 State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, College of Life Sciences, Nankai University, Tianjin, China 2 College of Life Sciences, Nankai University, Tianjin, China 3 Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China * These authors have contributed equally to this work Correspondence to: Cheng Yang, email: cyang66_2001@yahoo.com Honggang Zhou, email: honggang.zhou@vip.126.com Tao Sun, email: sunrockmia@hotmial.com Keywords: DHA; AIT; CXCR3; PI3K; NF-κB Received: September 19, 2017 Accepted: November 13, 2017 Published: December 01, 2017 ABSTRACT Dihydroartemisinin (DHA) is the first generation of naturally occurring artemisinin derivatives with antimalarial activity. Recent research showed that this drug also features immunosuppressive and anti-inflammatory properties. Autoimmune thyroiditis (AIT) is a common organ-specific autoimmune disease with no available effective drug treatment. In this study, we investigated effects of DHA on AIT in vitro and in vivo . Results showed that DHA can visibly reduce antithyroglobulin antibody and thyroid peroxidase antibody levels and regulate T helper cells (Th) 1/Th2 imbalance of experimental AIT mice. DHA also dose-dependently suppressed proliferation of lymphocytes induced by lipopolysaccharide and concanavalin A. DHA inhibited binding of C-X-C chemokine ligand 10 (CXCL10) and its receptor (C–X–C motif) receptor 3 (CXCR3), thus inhibiting calcium flow. DHA can also reduce expression levels of PI3-kinase (PI3K), p-PI3K, protein kinase B (AKT), p-AKT, nuclear factor (NF)-κB/p65, and p-NF-κB/p65. In conclusion, DHA may serve as treatment drug for AIT by inhibiting the CXCR3/PI3K/AKT/NF-kB signaling pathway.
Remote sensing monitoring of alpine grassland nutritional status is a key factor of grassland reasonable utilization, also a difficulty for dynamic vegetation monitoring. The present paper studies the correlations between vegetation nutrition and hyperspectral data. The results showed that two band ratio models have a significant correlation with biomass, air-DM, P, CF, and CP. MAXR models have a significant correlation with most of nutrition index when selected wavebands equaled five. On the whole, the MAXR model precedes two band ratio models. Using MAXR models to estimate air-DM, P and CF can obtain higher accuracy.
// Xiao-Yu Ai 1, * , Yuan Qin 1, 2, * , Hui-Jua Liu 2, * , Zhan-Hong Cui 1, 2 , Meng Li 1, 2 , Jia-Huan Yang 1, 2 , Wei-Long Zhong 1, 2 , Yan-Rong Liu 2 , Shuang Chen 2 , Tao Sun 1, 2 , Hong-Gang Zhou 1, 2 and Cheng Yang 1, 2 1 State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, China 2 Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China * These authors have contributed equally to this work Correspondence to: Cheng Yang, email: Cheng.yang@nankai.edu.cn Hong-Gang Zhou, email: honggang.zhou@vip.126.com Keywords: apigenin; IBD; CAC; NF-κB; STAT3 Received: July 04, 2017 Accepted: August 17, 2017 Published: October 27, 2017 ABSTRACT Apigenin is a naturally occurring compound with anti-inflammatory, antioxidant, and anticancer properties. Here, we investigated the effects of apigeninin inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Apigenin effectively inhibited ulcerative colitis, a type of IBD, and CAC. Apigenin decreased myeloperoxidase (MPO), inflammatory cytokine and COX-2 levels, and it attenuated inflammatory cell infiltration in treated colon tissues as compared to untreated model colon tissues. Apigenin also reduced NF-κB and STAT3 activity in vitro and in vivo , thereby inhibiting inflammation and inflammation-induced carcinogenesis. Thus apigenin appears to inhibit inflammation and inflammation-induced carcinogenesisin IBD and CAC by suppressing STAT3-NF-κB signaling.
Sesquiterpene lactones (SL) have a wide range of applications in anti-tumor and anti-inflammatory therapy. However, the pharmacological mechanism of such substances is not clear. In this study, parthenolide (PTL) was used as an example to explore the anti-tumor effect of natural molecules and their common mechanism. We showed that PTL inhibited the proliferation and migration by reverse EMT via the ERK2/NF-κB/Snail pathway in vivo and in vitro. Interestingly, Multiple potential targets of PTL contain a Gly-Leu-Ser/Lys-"co-adaptation pocket". This inspiring us analogies of PTL may also bind to these target proteins and play a similar function. Significantly, the Concept of co-adaptation pocket may help to increase the selectivity of drug research and development.
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