Search engine for discovering works of Art, research articles, and books related to Art and Culture
ShareThis
Javascript must be enabled to continue!

e0034 Inhibition of atorvastatin on the autophagy of vascular endothelial cells

View through CrossRef
Objective To explore the mechanism of atorvastatin's protection on vascular endothelial cells, we conducted the research of impact of atorvastatin on vascular endothelial cells autophagy in different times. Methods We used the Hank's to replace the normal medium to induce autophagy of vascular endothelial cells. In pre-inducement and induction procedure, the cells were incubated with normal medium which includes atorvastatin or not and Hank's, respectively. Experimental cells were randomly divided into four groups: control group (Group I), the group of pre-inducement with atorvastatin (Group II), the group of inducement with atorvastatin (Group III) and the group of pre-inducement and inducement both with atorvastatin (Group IV). Transmission electron microscope (TEM) was used to detect autophagy. The RT-PCR was employed to detect the autophagy-specific markers' (Beclin 1 and Map1lc3) expression in each group of cells. Results Compared with the group I, target genes (Beclin 1 and Map1lc3) of the group III and the group IV had a significant decreased expression (p<0.01). The expression of the group II were all lower than the group I (p>0.05). The group IV was better than the group III (p>0.05). Via TEM detection, the cells showed typical morphological change. There into, the proportions of preautophagosome to the total area of cytoplasm in group III and group IV are remarkably decreased than that of group I, and the difference was significant (p<0.01). The proportions of group II is lower than that of group I, but not significant (p>0.05). The proportions of group IV is lower than that of group III, but there was no obvious difference between two groups (p>0.05). Conclusion Using atorvastatin, in induction procedure, can inhibit vascular endothelial cells autophagy, which may be related to the role of atorvastatin's improvement on endothelial function. However, using atorvastatin, prior to the occurrence of induced autophagy, can not quite inhibit the occurrence of autophagy.
Title: e0034 Inhibition of atorvastatin on the autophagy of vascular endothelial cells
Description:
Objective To explore the mechanism of atorvastatin's protection on vascular endothelial cells, we conducted the research of impact of atorvastatin on vascular endothelial cells autophagy in different times.
Methods We used the Hank's to replace the normal medium to induce autophagy of vascular endothelial cells.
In pre-inducement and induction procedure, the cells were incubated with normal medium which includes atorvastatin or not and Hank's, respectively.
Experimental cells were randomly divided into four groups: control group (Group I), the group of pre-inducement with atorvastatin (Group II), the group of inducement with atorvastatin (Group III) and the group of pre-inducement and inducement both with atorvastatin (Group IV).
Transmission electron microscope (TEM) was used to detect autophagy.
The RT-PCR was employed to detect the autophagy-specific markers' (Beclin 1 and Map1lc3) expression in each group of cells.
Results Compared with the group I, target genes (Beclin 1 and Map1lc3) of the group III and the group IV had a significant decreased expression (p<0.
01).
The expression of the group II were all lower than the group I (p>0.
05).
The group IV was better than the group III (p>0.
05).
Via TEM detection, the cells showed typical morphological change.
There into, the proportions of preautophagosome to the total area of cytoplasm in group III and group IV are remarkably decreased than that of group I, and the difference was significant (p<0.
01).
The proportions of group II is lower than that of group I, but not significant (p>0.
05).
The proportions of group IV is lower than that of group III, but there was no obvious difference between two groups (p>0.
05).
Conclusion Using atorvastatin, in induction procedure, can inhibit vascular endothelial cells autophagy, which may be related to the role of atorvastatin's improvement on endothelial function.
However, using atorvastatin, prior to the occurrence of induced autophagy, can not quite inhibit the occurrence of autophagy.

Related Results

Abstract 1674: Inhibition of GSK3 reduces p70S6K activity and promotes autophagy independently of the JNK-cJun pathway.
Abstract 1674: Inhibition of GSK3 reduces p70S6K activity and promotes autophagy independently of the JNK-cJun pathway.
Abstract Considering that a tumor promoting role for GSK3 has been suggested in pancreatic cancer (PC) cells and that GSK3 inhibitors are currently under clinical tr...
Effect of exosomes from nasopharyngeal carcinoma on endothelium pyroptosis and metastasis.
Effect of exosomes from nasopharyngeal carcinoma on endothelium pyroptosis and metastasis.
93 Background: Nasopharyngeal carcinoma (NPC) is a malignant tumor occurring in the epithelium of nasopharyngeal mucosa. Radiotherapy can achieve a good therapeutic effect for NPC...
Identify and Assess Drug Interactions with Atorvastatin in Inpatient Care
Identify and Assess Drug Interactions with Atorvastatin in Inpatient Care
Background: Atorvastatin is a recent HMG-COA reductase inhibitor used to treat primary hypercholesterolemia, homozygous familial hypercholesterolemia, and mixed dyslipidemias. It i...
Abstract 1688: Autophagy inhibition enhances the antitumor effects of combretastatin A4 phosphate (CA4P).
Abstract 1688: Autophagy inhibition enhances the antitumor effects of combretastatin A4 phosphate (CA4P).
Abstract Vascular disruptive agents such as CA4P cause an acute shutdown of the tumor vasculature resulting in metabolic stress and central tumor necrosis. However, ...
Data from Autophagy Supports Breast Cancer Stem Cell Maintenance by Regulating IL6 Secretion
Data from Autophagy Supports Breast Cancer Stem Cell Maintenance by Regulating IL6 Secretion
<div>Abstract<p>Autophagy is a mechanism by which cells degrade cellular material to provide nutrients and energy for survival during stress. The autophagy is thought t...
Data from Autophagy Supports Breast Cancer Stem Cell Maintenance by Regulating IL6 Secretion
Data from Autophagy Supports Breast Cancer Stem Cell Maintenance by Regulating IL6 Secretion
<div>Abstract<p>Autophagy is a mechanism by which cells degrade cellular material to provide nutrients and energy for survival during stress. The autophagy is thought t...
Reelin engages non-canonical signaling pathways to drive endothelial remodeling and plasticity
Reelin engages non-canonical signaling pathways to drive endothelial remodeling and plasticity
Abstract BACKGROUND The vascular endothelium is a dynamic tissue central to vascular homeostasis and disease, with endothelial ...
Cytotoxicity of arginine deprivation to AML cells is mediated by autophagy / by Fatima Taki . (c2020)
Cytotoxicity of arginine deprivation to AML cells is mediated by autophagy / by Fatima Taki . (c2020)
In this study, we assess the activation of autophagy in AML cells following arginine deprivation, the mechanism of its activation, and its impact on cell cytotoxicity. Arginine dep...

Back to Top