Effects of rosiglitazone on MCP-1, COX-2 and NF-κB expressions in spontaneously hypertensive rats

Objective: To investigate the expressions of inflammatory factors including NF-κB, COX-2 and MCP-1 as well as the changes of neurons in the hippocampus of spontaneously hypertensive rats (SHRs) so as to explore the protective effect of peroxisome proliferator-activated receptor γ (PPARγ) agonists on hypertension-induced brain injury and the related mechanisms. Methods: Male SHR and WKY rats aged 56 weeks were divided evenly into two groups at random: control group (2 mL/d saline by lavage) and Ros group [5 mg/(kg·d) rosiglitazone dissolved in 2 mL saline by lavage]. The animals were killed at week 64 before SBP test and their brains were taken out for detection. Then Nissl's staining was performed in CA1 area; COX-2 and MCP-1 mRNA expressions were detected by Real time PCR, while NF-κB and PPARγ protein expressions were detected by Western blot. Results: We found in the SHRs a decreased expression of PPARγ; upregulated expressions of NF-κB, MCP-1 and COX-2 (P<0.05); and decreased number of neurons in CA1 subfield of the hippocampus (P<0.05). Rosiglitazone reversed these pathological changes and exerted neuroprotective effects through PPARγ pathway. Conclusion: In SHRs there is obvious loss of neurons in CA1 subfield of the hippocampus. The expressions of inflammatory factors like NF-κB, MCP-1 and COX-2 are upregulated, which may be involved in the pathologic process of hypertension-induced neuronal injury. Rosiglitazone can have anti-inflammatory and neuroprotective effects by activating PPAR-γ pathway.