Objectives
Psoriasis is an autoimmune, inflammatory disease that needs a reliable animal model. Imiquimod (IMQ)-induced psoriasis is a widely used preclinical tool for psoriasis research. However, this model is sensitive to the genetic variation of mice. The present study explores mice’s genetic background on disease stability and severity induced by IMQ.
Methods
Three distinct strains of mice (Balb/c, C57BL/6, and Swiss albino) were divided into four groups (Vaseline, IMQ, IMQ+Clobetasol, and IMQ+Curcumin). Psoriasis area severity index (PASI) score, ear/back skin thickness, body weight alterations, and histopathological examination were employed to analyze disease severity. The spleen index studied the systemic effect. Strain effect on oxidative stress induced by IMQ was evaluated by estimating antioxidant factors, superoxide dismutase (SOD), catalase, and glutathione (GSH).
Results
IMQ application resulted in increased PASI score, thickness, and alterations in body weight, confirming disease development in all the mice. However, the disease stability/severity between these strains was not identical. Although IMQ application caused splenomegaly, IMQ+curcumin treated C57BL/6 mice demonstrated a synergistic effect of IMQ and curcumin on the spleen resulting in increased splenomegaly. Decreased cellular enzyme activity in SOD, Catalase, and levels of GSH was observed in IMQ challenged mice, indicating the participation of the redox system in the genesis of the disease that was comparable among the strains.
Conclusions
These results indicate the existence of strain-dependent development of the disease. The Swiss model was found to be better in terms of disease severity and stability than other models. Further, a detailed mechanistic study might help to explain the pathological difference between these strains.
Introduction The influence of animal strain on psoriasis model development by imiquimod (IMQ) has been studied in Balb/c and Swiss mice.
Materials and Methods Female mice of either strain were challenged with 5% IMQ (62.5 mg on back skin, 10 mg on right ear). They were observed for the severity of the disease using Psoriasis area severity index (PASI), splenomegaly, and histopathological alterations. To validate the model, well-established antipsoriatic drug clobetasol (0.05%, 120 mg on the back skin, 10 mg on the right ear) was used. Additionally, to study the strain-dependent response to IMQ associated with oxidative stress, various antioxidant factors like superoxide dismutase (SOD), catalase (CT), and glutathione (GSH) were measured. Antioxidant natural product curcumin (1%, 150 mg on back skin, 12.5 mg on right ear) was used to evaluate the alleviation of oxidative stress on distinct mice strain.
Results PASI score, body weight, and histopathology indicated the development of disease in both the strains, severity, and stability of which was dependent on the particular strain. Splenomegaly suggested the systemic effect, which was comparable in both the stains. IMQ and its involvement in redox status were confirmed by an alteration in the activity of SOD, CT, and levels of GSH.
Conclusion This study demonstrated that, in the IMQ-induced psoriasis model, the genetic background has some impact on the disease severity, stability, and redox imbalance.
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