Examination of the molecular mechanism of the mutual inhibitory effect of each cytotoxicity caused by the combined extraction of Coptidis Rhizoma and Rhei Rhizoma : An example of providing evidence for ‘herbal pair’ theory

2021 ◽  
Author(s):  
Rena Suzuki ◽  
Qingfeng Zhao ◽  
Haruka Hosokai ◽  
Michihisa Tohda
Keyword(s):  
Molecular Mechanism ◽  
Inhibitory Effect ◽  
Rhei Rhizoma ◽  
Coptidis Rhizoma

scholarly journals The Effects ofChunghyul-Dan(A Korean Medicine Herbal Complex) on Cardiovascular and Cerebrovascular Diseases: A Narrative Review

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Woo-Sang Jung ◽  
Seungwon Kwon ◽  
Seung-Yeon Cho ◽  
Seong-Uk Park ◽  
Sang-Kwan Moon ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Ethanol Extract ◽  
Inhibitory Effect ◽  
Cerebrovascular Diseases ◽  
Stroke Recurrence ◽  
Neuroprotective Effects ◽  
Clinical Safety ◽  
Endogenous Catecholamine ◽  
Rhei Rhizoma ◽  
Coa Reductase

Chunghyul-dan(CHD) is a herbal complex containing 80% ethanol extract and is composed ofScutellariae Radix,Coptidis Rhizoma,Phellodendri Cortex,Gardeniae Fructus, andRhei Rhizoma. We have published several experimental and clinical research articles on CHD. It has shown antilipidemic, antihypertensive, antiatherosclerotic, and inhibitory effects on ischemic stroke recurrence with clinical safety in the previous studies. The antilipidemic effect of CHD results from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and pancreatic lipase-inhibitory activity. The antihypertensive effect likely results from the inhibitory effect on endogenous catecholamine(s) release and harmonization of all components showing the antihypertensive effects. Furthermore, anti-inflammatory and antioxidant effects on endothelial cells are implicated to dictate the antiatherosclerotic effects of CHD. It also showed neuroprotective effects on cerebrovascular and parkinsonian models. These effects of CHD could be helpful for the prevention of the recurrence of ischemic stroke. Therefore, we suggest that CHD could be a promising medication for treating and preventing cerebrovascular and cardiovascular diseases. However, to validate and better understand these findings, well-designed clinical studies are required.

Urea inhibits hypertonicity-inducible TonEBP expression and action

2001 ◽  
Vol 280 (5) ◽  
pp. F904-F912 ◽  
Author(s):  
Wei Tian ◽  
David M. Cohen
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanism ◽  
Reporter Gene ◽  
Gene Transcription ◽  
Phorbol Ester ◽  
Renal Medulla ◽  
Inhibitory Effect ◽  
Characteristic Set ◽  
Enhancer Element ◽  
Enhancer Binding Protein

Tonicity-responsive genes are regulated by the TonE enhancer element and the tonicity-responsive enhancer binding protein (TonEBP) transcription factor with which it interacts. Urea, a permeant solute coexistent with hypertonic NaCl in the mammalian renal medulla, activates a characteristic set of signaling events that may serve to counteract the effects of NaCl in some contexts. Urea inhibited the ability of hypertonic stressors to increase expression of TonEBP mRNA and also inhibited tonicity-inducible TonE-dependent reporter gene activity. The permeant solute glycerol failed to reproduce these effects, as did cell activators including peptide mitogens and phorbol ester. The inhibitory effect of urea was evident as late as 2 h after the application of hypertonicity. Pharmacological inhibitors of known urea-inducible signaling pathways failed to abolish the inhibitory effect of urea. TonEBP action is incompletely understood, but evidence supports a role for proteasome function and p38 action in regulation; urea failed to inhibit proteasome function or p38 signaling in response to hypertonicity. Consistent with its effect on TonEBP expression and action, urea pretreatment inhibited the effect of hypertonicity on expression of the physiological effector gene, aldose reductase. Taken together, these data 1) define a molecular mechanism of urea-mediated inhibition of tonicity-dependent signaling, and 2) underscore a role for TonEBP abundance in regulating TonE-mediated gene transcription.

The molecular mechanism of fullerene-inhibited aggregation of Alzheimer's β-amyloid peptide fragment

Nanoscale ◽  
2014 ◽  
Vol 6 (16) ◽  
pp. 9752-9762 ◽  
Author(s):  
Luogang Xie ◽  
Yin Luo ◽  
Dongdong Lin ◽  
Wenhui Xi ◽  
Xinju Yang ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Inhibitory Effect ◽  
Amyloid Peptide ◽  
Peptide Fragment ◽  
Experiment Study ◽  
Simulation And Experiment ◽  
Β Amyloid ◽  
Combined Simulation ◽  
Β Amyloid Peptide ◽  
Β Sheet

A combined simulation and experiment study demonstrates that fullerenes inhibit the β-sheet formation of Aβ(16–22) and fullerene hexagonal rings play a significant role on the inhibitory effect.

scholarly journals Molecular Mechanism of the Inhibitory Effect of Aldosterone on Endothelial NO Synthase Activity

Hypertension ◽  
2006 ◽  
Vol 48 (1) ◽  
pp. 165-171 ◽  
Author(s):  
Daisuke Nagata ◽  
Masao Takahashi ◽  
Kuniko Sawai ◽  
Tetsuya Tagami ◽  
Takeshi Usui ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Inhibitory Effect ◽  
No Synthase ◽  
Endothelial No Synthase

Inhibitory effect of arsenic trioxide on neuronal migration in vitro and its potential molecular mechanism

2015 ◽  
Vol 40 (3) ◽  
pp. 671-677 ◽  
Author(s):  
Hao Zhou ◽  
Ye Liu ◽  
Xin-Jie Tan ◽  
Yu-Chuan Wang ◽  
Kai-Yu Liu ◽  
...  
Keyword(s):  
Arsenic Trioxide ◽  
Molecular Mechanism ◽  
Neuronal Migration ◽  
Inhibitory Effect
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