Deciphering the Q-markers of nourishing kidney-yin of Cortex Phellodendri amurense from ZhibaiDihuang pill based on Chinmedomics strategy

Phytomedicine ◽  
2021 ◽  
pp. 153690
Author(s):  
Shao-bo Liu ◽  
Sheng-wen Lu ◽  
Hui Sun ◽  
Ai-hua Zhang ◽  
Hui Wang ◽  
...  
Keyword(s):  
Planta Medica ◽  
2016 ◽  
Vol 83 (03/04) ◽  
pp. 277-284 ◽  
Author(s):  
Ling Wang ◽  
Xue Wang ◽  
Xiao-Ming Zhu ◽  
Yan-Qi Liu ◽  
Wen-Juan Du ◽  
...  

2012 ◽  
Vol 518-523 ◽  
pp. 1913-1917
Author(s):  
Fang Qin Guo ◽  
Wei Chen

The effects of N deposition induced by environmental pollution on litter decomposition rate in Shenyang city are analyzed by the reciprocal transplant experiment. By contrasting environments and intraspecific variations in Cortex Phellodendri Chinensis leaf litter quality on mass loss rates to investigate the effects of N deposition on mass loss rates in urban and suburb. The results showed that N deposition in urban significantly affected litter decomposition rate by affecting litter quality and environmental conditions. There was a faster decomposition rate when the environmental conditions or litter quality was affected by N deposition.


2021 ◽  
Vol 8 (10) ◽  
Author(s):  
Chen G ◽  
◽  
Liu Y ◽  
Zhang M ◽  
Xu Y ◽  
...  

Niloticin is an active compound from Cortex phellodendri, but its antiinflammatory activity has not yet been explored. The aim of the present study was to assess the drug potential of niloticin and to study the MD-2-targeting mechanism of its anti-inflammatory activity. Niloticin’s drug potential was analyzed using the Traditional Chinese Medicine Systems Pharmacology Database. Molecular docking and biolayer interferometry technology were used to explore the anti-inflammatory mechanism of niloticin by targeting myeloid differentiation protein 2 (MD-2), which mediates a series of Toll-Like Receptor (TLR) 4-dependent inflammatory responses. The cytokines involved in the LPSTLR4/ MD-2-NF-κB pathway were evaluated by ELISA, RT-PCR, and western blot. The results showed that niloticin has drug potential and could bind to MD- 2. Niloticin had no impact on cell viability. Niloticin could significantly decrease the levels of NO, IL-6, TNF-a, and IL-1β (P<0.01) induced by LPS. IL-1β, IL-6, iNOS, TNF-a, and COX-2 mRNA expression levels were decreased by niloticin (all P<0.01). Compared with the control group, TLR4, p65, MyD88, p-p65, and iNOS expression levels induced by LPS were suppressed by niloticin (all P<0.01). In conclusion, niloticin is a potential MD-2 antagonist. It might interact with MD-2 to play an anti-inflammatory role by suppressing the activation of the LPS-TLR4/MD-2-NF-κB signaling pathway.


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