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[Effect of dexamethasone on spontaneously apoptosis of polymorphonuclear neutrophils from postburn rabbits]
Pi-hong Zhang1, Liu-rong Yang, Xiao-yuan Huang
1Department of Burns & Plastic Surgery, Xiangya Hospital, Central South University, Changsha 410008, China.
Objective:
To study the effect of dexamethasone on spontaneously apoptosis, bcl-2, and neuclear facor kappa (NFkappaB) expressions of polymorphonuclear neutrophil (PMN) from postburn rabbits.
Methods:
PMN were isolated from 8 rabbits on 24 postburn hours and cultured with normal serum (NS), burn serum (BS), normal serum plus dexamethasone (ND), and burn serum plus dexamethasone (BD) for 24 hours, respectively. The quantification of apoptosis was analyzed by acridine orange + ethidium bromide fluorescent staining and flow cytometry , and the contents of bcl-2 and NFkappaB protein detected by immunohistochemical method.
Results:
In the BS group, the percentage of apoptotic PMN decreased (compared with NS group, 6.18 +/- 0.96 vs. 21.77 +/- 2.32, P<0.05), and the contents of bcl-2 and NFkappaB protein increased (compared with NS group, 83.27 +/- 5.45 vs. 49.95 +/- 2.67, P<0.05). When compared with BS group, the apoptotic percentage of BD group increased (12.67 +/- 0.71 vs. 6.18 +/- 0.96, P<0.05), and the content of NFkappaB protein reduced (0. 1031 +/- 0.0154 vs. 0.1802 +/- 0.0130, P<0.05), but no significant difference between ND and NS group was found.
Conclusion:
Dexamethasone decreases the inhibition of PMN apoptosis by bumn serum, which may be associated with the down-regulation of NFKB expression.
Insights
Dexamethasone treatment reduced burn serum-induced inhibition of polymorphonuclear neutrophil (PMN) apoptosis in rabbits. This effect may be linked to decreased nuclear factor kappa B (NFκB) expression.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Context:
- Burn injury triggers complex inflammatory responses.
- Polymorphonuclear neutrophils (PMNs) play a critical role in burn wound healing and inflammation.
- Dysregulated PMN apoptosis contributes to prolonged inflammation post-burn.
Purpose:
- To investigate the impact of dexamethasone on PMN apoptosis in a rabbit burn model.
- To assess the effects of dexamethasone on bcl-2 and nuclear factor kappa B (NFκB) expression in PMNs.
- To elucidate the molecular mechanisms underlying dexamethasone's action on PMN behavior post-burn.
Summary:
- Burn serum (BS) significantly decreased PMN apoptosis and increased bcl-2 and NFκB expression compared to normal serum (NS).
- Dexamethasone treatment (BD group) increased PMN apoptosis and reduced NFκB expression compared to the BS group.
- No significant changes in PMN apoptosis or protein expression were observed between normal serum plus dexamethasone (ND) and NS groups.
Impact:
- Dexamethasone mitigates the inhibitory effect of burn serum on PMN apoptosis.
- The anti-apoptotic effect of dexamethasone in burn serum appears to be mediated by the down-regulation of NFκB.
- Findings suggest a potential therapeutic role for dexamethasone in managing burn-related inflammation by modulating PMN apoptosis.
