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[THE EFFECT OF OF POLY(ADP-RIBOSE) POLYMERASE INHIBITOR 4-HYDROXY-QUINAZOLINE ON DEATH OF IMMUNE CELLS UNDER IMMUNE
Abstract:
The influence of poly(ADP-ribose) polymerase (PARP) in- hibitor 4-hydroxyquinazoline (4-HQ) on the level of DNA damage and on the death of thymic and lymph node cells in mouse model of immune complex injury was investigated to reveal its possible cytoprotective effect. As shown by comet assay, DNA damage index of immune cells was increased 4,0 times in mice with immune complex-mediated pathology induced by a long-term immunization of CBA mice with bovine serum albumin (BSA), P<0,001. The percentage of thymic cells with strong DNA damage was increased to 77% under immunization (compared to 1,5% in control mice) and the percentage of such cells from lymph nodes was increased to 80% (compared to 0% in control), in both cases P< 0,001. Genotoxic stress was reduced by treatment of immunized mice with 4-HQ: the percentage of lymphocytes with strong DNA damage was significantly decreased that promoted increase in the amount of cells having intact DNA. PARP inhibition exerted a strong cytoprotective effect: viability of thymus and lymph node cells was increased mainly due to reduced level of necrosis. So, our results suggest that PARP may be involved in thymic and lymph node cell damage in immune complex mediated pathology and give evidence that inhibition of this enzyme may constitute a perspective target in immune complex diseases prevention and therapy.
Insights
Poly(ADP-ribose) polymerase (PARP) inhibitor 4-hydroxyquinazoline (4-HQ) reduced DNA damage and cell death in mice with immune complex injury. PARP inhibition shows potential for preventing and treating immune complex diseases.
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- Immune complex-mediated pathology can lead to significant DNA damage and cell death in immune cells.
- Poly(ADP-ribose) polymerase (PARP) is implicated in cellular responses to DNA damage.
Purpose of the Study:
- To investigate the cytoprotective effect of the PARP inhibitor 4-hydroxyquinazoline (4-HQ) in a mouse model of immune complex injury.
- To assess the impact of 4-HQ on DNA damage and cell viability in thymic and lymph node cells.
Main Methods:
- Induction of immune complex pathology in CBA mice via long-term immunization with bovine serum albumin (BSA).
- Comet assay to quantify DNA damage index in immune cells.
- Assessment of thymic and lymph node cell viability and necrosis.
- Treatment of immunized mice with the PARP inhibitor 4-HQ.
Main Results:
- Immune complex pathology significantly increased DNA damage in immune cells (4.0-fold increase).
- The percentage of thymic and lymph node cells with strong DNA damage increased to 77% and 80%, respectively.
- 4-HQ treatment reduced genotoxic stress, decreasing DNA-damaged lymphocytes and increasing cells with intact DNA.
- PARP inhibition demonstrated a strong cytoprotective effect, increasing cell viability primarily by reducing necrosis.
Conclusions:
- PARP plays a role in thymic and lymph node cell damage during immune complex-mediated pathology.
- Inhibition of PARP by 4-HQ offers a potential therapeutic strategy for preventing and treating immune complex diseases.
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