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Rosuvastatin can block pro-inflammatory actions of transgenic human C-reactive protein without reducing its
Jan Šilhavý1, Václav Zídek, Vladimír Landa
1Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Insights
Rosuvastatin reduces inflammation and heart damage by blocking human C-reactive protein (CRP) effects, independent of lowering CRP levels. This study shows statins offer cardiovascular protection beyond reducing CRP.
Area of Science:
- Cardiovascular Science
- Pharmacology
- Inflammation Research
Background:
- Statins possess anti-inflammatory properties and reduce cardiovascular event risk.
- C-reactive protein (CRP) is a biomarker for inflammation and heart disease.
- The independent effect of statins on CRP's pro-inflammatory actions is not well understood.
Purpose of the Study:
- To investigate if rosuvastatin can block pro-inflammatory effects of human CRP.
- To determine if this effect is independent of reducing circulating human CRP levels.
Main Methods:
- Studied rosuvastatin's anti-inflammatory effects in spontaneously hypertensive rats (SHR) genetically engineered to express human CRP (CRP-transgenic SHR) and in nontransgenic SHR.
- Measured circulating levels of inflammatory markers (IL6, TNFα), cardiac inflammation, oxidative damage, and adipose tissue parameters.
Main Results:
- Rosuvastatin decreased IL6 and TNFα in CRP-transgenic SHR without lowering human CRP levels.
- In contrast, rosuvastatin had minimal effect on IL6 and TNFα in nontransgenic SHR.
- Rosuvastatin significantly reduced cardiac inflammation, oxidative damage, and improved adipose tissue function more in CRP-transgenic SHR.
Conclusions:
- Rosuvastatin provides protection against human CRP's pro-inflammatory effects.
- This protective mechanism is independent of the drug's ability to reduce circulating human CRP levels.
Aims:
Statins have antiinflammatory effects and are known to decrease risk of cardiovascular events and to reduce serum levels of C-reactive protein (CRP), a widely studied biomarker and potential mediator of inflammation and heart disease. However, it is unclear whether statins can block pro-inflammatory effects of human CRP independent of their ability to reduce serum levels of human CRP. Here, we investigated whether rosuvastatin could block pro-inflammatory effects of human CRP without reducing circulating levels of human CRP.
Methods And Results:
We studied the antiinflammatory effects of rosuvastatin in spontaneously hypertensive rats (SHR) transgenically expressing human CRP (CRP-transgenic SHR) and in nontransgenic SHR lacking human CRP (nontransgenic SHR). The CRP-transgenic SHR is characterized by increased serum levels of human CRP and inflammation. In the CRP-transgenic strain, we found that rosuvastatin treatment decreased circulating levels of inflammatory response markers IL6 and TNFα without decreasing circulating levels of human CRP. In contrast, in the nontransgenic strain lacking human CRP, rosuvastatin treatment had little or no effect on IL6 and TNFα levels. Rosuvastatin also reduced cardiac inflammation and oxidative tissue damage, reduced epididymal fat mass, and improved adipose tissue lipolysis much more in the CRP-transgenic strain than in the nontransgenic strain.
Conclusion:
Rosuvastatin can protect against pro-inflammatory effects of human CRP in a manner that is not dependent on achieving a reduction in circulating levels of human CRP.
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