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[The effect of complement C3a receptor antagonist in the kidney immune injury in trichloroethylene-sensitized mice]
1Department of Occupational and Environment Health, School of Public Health, Anhui Medical University, Hefei 230032, China.
Abstract:
Objective: To explore the effect of complement C3 a-C3a receptor in the kidney immune inju-ry in trichloroethylene-sensitized mice by using C3a receptor specific antagonist C3aRA and discuss the patho-genesis of kidney injury in occupational dermatitis medicamentosa-like of trichloroethylene (ODMLT) . Methods: 42 female 6~8 weeks old BALB/c mice of specific pathogen free were randomly divided into blank control group (5) , solvent control group (5) , TCE treatment group (16) and TCE+C3aRA treatment group (16) . The TCE treat-ment group and TCE+C3aRA treatment group were further divided into the sensitized group and the non-sensi-tized group according to the skin sensitization test score. Renal function was detected by biochemical detection kit; expression of C3aR in kidney tissue was detected by qPCR; expression of IL-1β and TNF-α protein were de-tected by immunohistochemical. Results: Compared with solvent control group and corresponding non-sensitized group, CRE and BUN in TCE sensitized group and TCE + C3aRA sensitized group were significantly increased (P<0.05) . Compared with TCE sensitized group, CRE and BUN in TCE+C3aRA sensitized group were signifi-cantly decreased (P<0.05) . Compared with solvent control group and TCE non-sensitized group, the expression level of C3aR gene in kidney tissue in TCE sensitized group was significantly increased (P<0.05) . There was a large number of IL-1β and TNF-α protein expression in kidney tissue in TCE sensitized group and TCE+C3aRA sensitized group. Compared with the TCE sensitized group, the expression level of IL-1β and TNF-α protein in kidney tissue in TCE+C3aRA sensitized group was significantly decreased (P<0.05) . Conclusion: C3a-C3aR may be involved in the kidney immune injury in TCE sensitized mice, C3aRA has a protective effect on the kid-ney immune injury in TCE sensitized mice.
Insights
Trichloroethylene (TCE) exposure can cause kidney immune injury, involving complement C3a-C3a receptor. Blocking this receptor with C3aRA offers a protective effect against TCE-induced kidney damage in mice.
Area of Science:
- Immunology
- Nephrology
- Toxicology
Background:
- Trichloroethylene (TCE) exposure is linked to occupational dermatitis medicamentosa-like (ODMLT) kidney injury.
- The role of complement C3a-C3a receptor (C3aR) in TCE-induced kidney damage is not fully understood.
Purpose of the Study:
- To investigate the involvement of the C3a-C3aR pathway in kidney immune injury in TCE-sensitized mice.
- To evaluate the therapeutic potential of a C3a receptor specific antagonist (C3aRA) in mitigating TCE-induced kidney damage.
Main Methods:
- BALB/c mice were exposed to TCE and treated with C3aRA.
- Renal function markers (CRE, BUN) were assessed.
- C3aR gene expression in kidney tissue was quantified using qPCR.
- Pro-inflammatory cytokines (IL-1β, TNF-α) were measured via immunohistochemistry.
Main Results:
- TCE sensitization significantly increased CRE and BUN levels, indicating impaired renal function.
- C3aR gene expression was elevated in the kidneys of TCE-sensitized mice.
- TCE sensitization led to increased expression of IL-1β and TNF-α proteins in kidney tissue.
- Treatment with C3aRA significantly reduced CRE, BUN, IL-1β, and TNF-α levels compared to TCE-sensitized mice.
Conclusions:
- The C3a-C3aR pathway plays a significant role in mediating kidney immune injury following TCE sensitization.
- C3aRA demonstrates a protective effect against TCE-induced kidney immune injury in a mouse model.
- Targeting the C3a-C3aR pathway may represent a viable therapeutic strategy for TCE-related nephrotoxicity.
