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[Study of Berberine on Attenuating PM2.5-Induced Vascular Endothelial Cells Injury by ERK1/2 Signal Pathway]
Objective:
To investigate the effect and mechanism of berberine in attenuating PM2. 5-induced human umbilical vein endothelial cells EA. hy926 injury.
Methods:
The samples of fine particulate matter( PM2. 5) were collected and made into suspension. Different concentrations of PM2. 5( 0,20,200,400 mg / L) were added into EA. hy926 cells for 24 h. The viability of EA. hy926 cells was detected by MTT assay, and apoptosis of EA. hy926 cells was detected by flow cytometry, the expressions of p-ERK1 /2,BAX and BCL-2 in the EA. hy926 cells were measured by Western blot,the contents of IL-6,TNF-α were measured by ELISA, the content of MDA, and the activities of SOD and LDH in the EA. hy926 cells culture supernatant were measured, respectively. Different concentrations of berberine( 10,50,100 μmol / L) and PD98059( 20 μmol / L) was added into the EA. hy926 cells to observe the effect of berberine.
Results:
Compared with control group,PM2. 5 decreased the viability in a dose dependent manner, and significantly upgraded the protein levels of p-ERK1 /2 and BAX / BCL-2 ratio,PM2. 5 increased the apoptosis of EA. hy926 cells, and increased the contents of IL-6,TNF-α and MDA, increased the activity of LDH, and decreased SOD activity in the EA. hy926 cells( P < 0. 05). Compared with PM2. 5 group, berberine increased the viability of EA. hy926 cells in a dose dependent manner,PM2. 5 significantly downgraded the protein levels of p-ERK1 /2 and BAX / BCL-2 ratio, and decreased the apoptosis of EA. hy926 cells, decreased the contents of IL-6,TNF-α and MDA, and decreased the activity of LDH, and increased SOD activity in the EA. hy926 cells( P < 0. 05).
Conclusion:
Berberine attenuates PM2. 5-induced EA. hy926 cells injury by inhibiting ERK1 /2 pathway.
Insights
Berberine protects human umbilical vein endothelial cells from injury caused by fine particulate matter (PM2.5). It works by inhibiting the ERK1/2 pathway, reducing inflammation and cell death.
Area of Science:
- Endothelial cell biology
- Environmental toxicology
- Pharmacology
Background:
- Fine particulate matter (PM2.5) exposure is a significant environmental risk factor for cardiovascular diseases.
- Endothelial cells play a crucial role in vascular health, and PM2.5-induced injury contributes to endothelial dysfunction.
- Berberine, a natural alkaloid, has demonstrated various pharmacological properties, including anti-inflammatory and antioxidant effects.
Purpose of the Study:
- To investigate the protective effects of berberine against PM2.5-induced injury in human umbilical vein endothelial cells (EA.hy926).
- To elucidate the underlying mechanism of berberine's action, focusing on the involvement of the ERK1/2 signaling pathway.
Main Methods:
- EA.hy926 cells were exposed to different concentrations of PM2.5.
- Cell viability was assessed using MTT assay, and apoptosis was measured by flow cytometry.
- Protein expression levels of p-ERK1/2, BAX, and BCL-2 were determined by Western blot.
- Inflammatory markers (IL-6, TNF-α), oxidative stress marker (MDA), and antioxidant enzyme activity (SOD) were measured.
- Lactate dehydrogenase (LDH) activity was also assessed.
Main Results:
- PM2.5 exposure significantly reduced cell viability, increased apoptosis, and elevated levels of inflammatory cytokines (IL-6, TNF-α) and oxidative stress markers (MDA).
- PM2.5 upregulated the protein expression of p-ERK1/2 and the BAX/BCL-2 ratio, while decreasing SOD activity.
- Berberine treatment dose-dependently reversed these detrimental effects of PM2.5, improving cell viability and reducing apoptosis and inflammation.
- Berberine treatment also downregulated p-ERK1/2 and the BAX/BCL-2 ratio, and restored SOD activity.
Conclusions:
- Berberine effectively attenuates PM2.5-induced injury in human umbilical vein endothelial cells.
- The protective mechanism involves the inhibition of the ERK1/2 signaling pathway.
- Berberine holds potential as a therapeutic agent for mitigating PM2.5-related endothelial damage.
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