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| Effects of Atorvastatin on glycogen synthase kinase-3 in lymphocytes of carotid atherosclerotic plaques in patients with early chronic kidney disease |
| SUN Yinyi1 ZHANG Qingde2 LI Songhua3 QU Zhongsen4 |
1.Department of Neurology, East Branch of Shanghai Sixth People′s Hospital Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai 201306, China;
2.Department of Physician, Heze Medical College, Shandong Province, Heze 274000, China;
3.Department of Radiology, East Branch of Shanghai Sixth People′s Hospital Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai 201306, China;
4.Department of Rehabilitation, East Branch of Shanghai Sixth People′s Hospital Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai 201306, China |
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Abstract Objective To explore the effects of Atorvastatin on glycogen synthase kinase-3 (GSK-3) in lymphocytes of carotid plaques in patients with early chronic kidney disease (CKD). Methods One hundred and forty-three patients with CKD 1-2 and carotid plaque from January to October 2017 in East Branch of Shanghai Sixth People′s Hospital Affiliated to Shanghai University of Medicine & Health Sciences and Heze Municipal Hospital were enrolled and divided into CKD group (76 cases) and treatment group (67 cases) according to random number table method. At the same time, 50 normal people over the age of 42 years were selected as the control group. The treatment group received oral Atorvastatin 20 mg/night. After 6 months of treatment, the activity and expression changes of GSK-3β and GSK-3β at Ser9 in peripheral blood lymphocytes of patients at different time points were observed. The GSK-3 activity was measured by 32P liquid scintillography for incorporated radioactivity, and the phosphorylation of GSK-3β at Ser9 and the total GSK-3β were determined by Western blot. Results Before treatment, compared with the control group, the carotid intima-media thickness (IMT) was significantly thicker (P ＜ 0.01), and the activity of GSK-3β was significantly decreased (P ＜ 0.01), and the phosphorylation of GSK-3β at Ser9 was significantly increased in lymphocytes in CKD group (P ＜ 0.01). When the treatment group treated with Atorvastatin for 6 months, the thickened IMT was reversed (P ＜ 0.05), and the activity of GSK-3 was resumed (P ＜ 0.01), and the phosphorylation of GSK-3β at Ser9 was decreased as compared with CKD group(P ＜ 0.01). Conclusion Lower activities of GSK-3 in lymphocytes of patients with early CKD might be associated with the formation and promotion of carotid atherosclerosis plaque. Atorvastatin might inhibit carotid atherosclerotic plaques by increasing activity of GSK-3 in phosphorylation of GSK-3β at Ser9.
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