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“Regression” of atherosclerosis in cell culture: Effects of stable prostacyclin analogues

Proceeding from the fact that the production of prostacyclin is decreased during atherosclerosis, which likely leads to the development of an atherosclerotic lesion, we assumed that addition of the exogenous prostacyclin would facilitate regression of atherosclerotic manifestations. To test this assumption we added stable prostacyclin analogues (carbacyclin and 6 β‐dihydro prostacyclin) to cells cultured from atherosclerotic lesions of human aorta. In primary culture, such cells retained the major manifestations of atherosclerosis at the cellular level, namely, enhanced proliferative activity and high lipid content. The stable prostacyclin analogues decreased the [3H]thymidine uptake into aortic cells by 1.5–2‐fold. These agents also substantially reduced the triglyceride and cholesteryl ester level in the cells cultured from atheorsclerotic lesions of aorta. In all these respects, carbacyclin was slightly more potent than 6 β‐dihydro prostacyclin. Thus, the stable prostacyclin analogues can inhibit proliferation and decrease the content of lipids in “atherosclerotic” cells, i.e., effect the “regression” of atherosclerosis at the arterial cell level. Apparently, these compounds may be regarded as potential antiatheroscelerotic drugs.