scholarly journals Loureirin B suppresses RANKL-induced osteoclastogenesis and ovariectomized osteoporosis via attenuating NFATc1 and ROS activities

Theranostics ◽  
2019 ◽  
Vol 9 (16) ◽  
pp. 4648-4662 ◽  
Author(s):  
Yuhao Liu ◽  
Chao Wang ◽  
Gang Wang ◽  
Youqiang Sun ◽  
Zhangrong Deng ◽  
...  
Keyword(s):  
2015 ◽  
Vol 37 (2) ◽  
pp. 666-676 ◽  
Author(s):  
Ting He ◽  
Xiaozhi Bai ◽  
Longlong Yang ◽  
Lei Fan ◽  
Yan Li ◽  
...  

Background/Aims: Our previous study confirmed that Loureirin B (LB) can inhibit hypertrophic scar formation. However, the mechanism of LB-mediated inhibition of scar formation is still unknown. Methods: Immunohistochemistry was used to detect expression of Col1, FN and TGF-β1 in skin and scar tissue. Fibroblasts were stimulated with TGF-β1 to mimic scar formation. LB or MAPK inhibitors were used to study the pathways involved in the process. Western blotting was used to evaluate the expression of p-JNK, p-ERK, p-p38, Col1 and FN. The contractile capacity of fibroblasts was evaluated using a gel contraction assay. Tissues were cultured ex vivo with LB to further investigate the participation of ERK and JNK in the LB-mediated inhibition of scar formation. Results: FN and Col1 were up regulated in hypertrophic scars. LB down regulated p-ERK and p-JNK in TGF-β1-stimulated fibroblasts, while levels of phosphorylated p38 did not change. The down regulation of p-ERK and p-JNK was associated with a reduction of Col1 and FN. Similarly, inhibition of ERK and JNK down regulated the expression of Col1 and FN in TGF-β1-stimulated fibroblasts. LB down regulated protein levels of p-ERK and p-JNK in cultured hypertrophic scar tissue ex vivo. Conclusions: This study suggests that LB can inhibit scar formation through the ERK/JNK pathway.


2017 ◽  
Vol 38 (7) ◽  
pp. 1038-1043 ◽  
Author(s):  
Yuelin Zhang ◽  
Yijie Sha ◽  
Kai Qian ◽  
Xu Chen ◽  
Qin Chen

2021 ◽  
Vol 12 ◽  
Author(s):  
Shujuan Shi ◽  
Qianru Zhao ◽  
Caihua Ke ◽  
Siru Long ◽  
Feng Zhang ◽  
...  

Loureirin B (LrB) is a constituent extracted from traditional Chinese medicine Resina Draconis. It has broad biological functions and an impressive immunosuppressive effect that has been supported by numerous studies. However, the molecular mechanisms underlying Loureirin B-induced immune suppression are not fully understood. We previously reported that Loureirin B inhibited KV1.3 channel, calcium ion (Ca2+) influx, and interleukin-2 (IL-2) secretion in Jurkat T cells. In this study, we applied CRISPR/Cas9 to edit KV1.3 coding gene KCNA3 and successfully generated a KV1.3 knockout (KO) cell model to determine whether KV1.3 KO was sufficient to block the Loureirin B-induced immunosuppressive effect. Surprisingly, we showed that Loureirin B could still inhibit Ca2+ influx and IL-2 secretion in the Jurkat T cells in the absence of KV1.3 although KO KV1.3 reduced about 50% of Ca2+ influx and 90% IL-2 secretion compared with that in the wild type cells. Further experiments showed that Loureirin B directly inhibited STIM1/Orai1 channel in a dose-dependent manner. Our results suggest that Loureirin B inhibits Ca2+ influx and IL-2 secretion in Jurkat T cells by inhibiting both KV1.3 and STIM1/Orai1 channels. These studies also revealed an additional molecular target for Loureirin B-induced immunosuppressive effect, which makes it a promising leading compound for treating autoimmune diseases.


2010 ◽  
Vol 24 (5) ◽  
pp. 547-557 ◽  
Author(s):  
Xu Chen ◽  
Jia-Ming Ma ◽  
Ke-Lan Yong ◽  
Jing-Ci Lv ◽  
Xia-Bing Zhang

The interaction between loureirin B (Lour B) and human serum albumin (HSA) was investigated by fluorescence and UV–vis absorption spectroscopy. Experimental results indicated that loureirin B had a strong ability to quench the intrinsic fluorescence of HSA through a dynamic quenching procedure. The fluorescence quenching data revealed that the quenching constants (KSV) 2.68×104, 3.30×104and 4.10×104l/mol at 300, 310 and 320 K, respectively. Based on the thermodynamic parameters obtained, the positive values of enthalpy change ΔH and entropy change ΔS suggested that hydrophobic forces played a major role in the interaction of Lour B with HSA. According to Förster theory of energy transfer, the distancerbetween HSA and Lour B was calculated to be 2.85 nm. Furthermore, the effect of Lour B on the conformation of HSA was analyzed by synchronous fluorescence and three-dimensional fluorescence spectra.


2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Xueliang Sun ◽  
Ke Wen ◽  
Zhizhong Xu ◽  
Zongqi He ◽  
Bensheng Wu ◽  
...  

Abstract Background Crohn’s disease (CD) is a chronic relapsing form of inflammatory bowel disease, seriously threatening human beings health. However, the pathogenesis of CD is still unclear and there is no specific effective drug for treatment of CD. Resina Donis (RD) obtained from Dracaena cochinchinensis (Lour.) S. C. Chen (Liliaceae), has been used for the treatment of CD clinically. Loureirin B (LB) is one of the most important chemical compositions and physiologically active ingredients of resina draconis. It has the molecular structure propan-1-one, 1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)-1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl) propan-1-one. The aim of this study was to investigate the effect of LB on CD and explore the underlying mechanisms. Methods and results In this study, the result demonstrated that LB prolonged the survival time of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rats and alleviated colonic damage in a dose dependent manner. Besides, LB remarkably ameliorated TNBS-induced inflammatory response via regulation of cytokines in the colonic tissues. Moreover, LB could reverse the established fibrosis and impede the accumulation infiltration, and improve the apoptosis induced by TNBS in a dose dependent manner. Further, LB dramatically suppressed TNBS-induced the activation of IL-6/STAT3/NF-κB signaling pathway. Conclusions These findings suggested that LB could be beneficial regarding ameliorating TNBS-induced CD, which may represent a novel approach to treat CD and provide an alternative choice for disorders associated with CD.


2018 ◽  
Vol 38 (6) ◽  
pp. 842-852
Author(s):  
Chen Su ◽  
Wan Ying ◽  
Liu Xiangming ◽  
Pan Xinxin
Keyword(s):  

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