scholarly journals Specificity Screening of Potential Active Components from Moutan Cortex for Rat Mesangial Cells HBZY-1 by Cell Membrane Immobilized Chromatography

2015 ◽  
Vol 06 (02) ◽  
pp. 147-157
Author(s):  
Junfei Gu ◽  
Minghua Zhang ◽  
Jiarui Yuan ◽  
Bingjie Zhao ◽  
Liang Feng ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Mesangial Cells ◽  
Active Components ◽  
Moutan Cortex

scholarly journals Leeches alleviates diabetic macroangiopathy by increasing nitric oxide production in rat aorta and restoring endothelium-dependent vasodilatation

2021 ◽  
Author(s):  
Zhaohui Fang ◽  
Xiu Hu ◽  
Zhi Chen ◽  
Jing Xie ◽  
Di Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Glucose ◽  
High Glucose ◽  
Mesangial Cells ◽  
Rat Aorta ◽  
Diabetic Rats ◽  
No Production ◽  
Active Components ◽  
Glucose Levels ◽  
Diabetic Macroangiopathy

IntroductionDiabetes mellitus (DM) is a chronic metabolic disorder characterized by elevated blood glucose level over a prolonged period, leading to severe damage in tissues including the heart, blood vessels, eyes and the kidneys. Danzhi Jiangtang Capsule (DJC) is an effective drug for diabetes, but the mechanism responsible for its efficacy remains unknown. This study aimed to explore the effective ingredient of DJC that ameliorated diabetes and the possible mechanisms.Material and methodsWe orally treated streptozotocin (STZ)-induced diabetic rats with 540 mg/kg DIC or the same dose of its four active components, namely Leeches, Pseudostellaria Polysaccharides (PP), Paeonia Suffruticosa Andr (PSA) and Rehmannia Glutinosa Libosch (RGL), respectively for 8 weeks.ResultsAlthough all of these components could reduce blood glucose levels in diabetic rats, the extent of alleviation of DJC was more pronounced than all of its four ingredients. Unlike the other three components, Leeches is the only effective ingredient of DJC that decreased tetrahydrobiopterin (BH4) oxidation to activate endothelial nitric oxide synthase (eNOS), and increased nitric oxide (NO) production, leading to improved endothelium-dependent relaxation both in diabetic rats and in immortalized human mesangial cells under the stimulation of high glucose.ConclusionsLeeches could alleviate diabetic macroangiopathy by inhibiting NO release in endothelial cells under high-glucose condition.

Extra- and intracellular metabolism of platelet-activating factor by cultured mesangial cells

1989 ◽  
Vol 256 (4) ◽  
pp. F735-F741
Author(s):  
R. Neuwirth ◽  
N. Ardaillou ◽  
D. Schlondorff
Keyword(s):  
Cell Membrane ◽  
Cell Surface ◽  
Phospholipase A2 ◽  
Mesangial Cells ◽  
Platelet Activating Factor ◽  
Outer Cell ◽  
Human Mesangial Cells ◽  
Rapid Inactivation ◽  
Outer Cell Membrane ◽  
Intracellular Metabolism

Metabolism of platelet-activating factor (PAF) was examined in cultured mesangial cells from human and rat glomeruli. Human mesangial cells, similar to those from rat, generated PAF after A23187. Both human and rat mesangial cells rapidly hydrolyzed [3H]PAF to lyso-[3H]PAF, and reacylated it into 1-alkyl-2-acyl glycerophosphocholine. Extra- and intracellular metabolism of PAF was then analyzed separately. The majority of [3H]PAF metabolism occurred extracellularly and generated Lyso-[3H]PAF. Intracellularly generated lyso-PAF was rapidly converted to 1-alkyl-2-acyl glycerophosphocholine. Cells prelabeled with [3H]PAF released some [3H]PAF within minutes and then rapidly converted it to lyso-PAF extracellularly. Under control conditions no acetylhydrolase activity was released from cells into the buffer. Acetylhydrolase activity could, however, be released from cell surface into buffer by limited trypsinization, supporting its location on the outer cell membrane. The acetylhydrolase activity was different from phospholipase A2, since phosphatidylcholine was not a substrate for the enzyme. In summary our results show that both rat and human mesangial cells can generate and metabolize PAF. Acetylhydrolase for PAF is present intracellularly, but also and predominantly on the outer cell surface of cells. This ectoenzymatic acetylhydrolase activity may be important in the rapid inactivation of PAF presented to cells, thus protecting cells from deleterious effects of PAF.

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