ObjectiveTo investigate the serum level of cystatin C (CysC), ischemia-modified albumin (IMA), and lipoprotein-associated phospholipase A2 (LP-PLA2) in patients with type 2 diabetes mellitus (T2DM) and with lower extremity atherosclerotic occlusive disease (LEASOD) and their correlation.MethodsFrom March 2017 to December 2019, 110 patients with T2DM with LEASOD, who were treated in our hospital, were selected as the observation group. One hundred ten healthy persons who received medical examination in our hospital during the same period were selected as the control group. Serum CysC, IMA, LP-PLA2, and ankle-brachial index (ABI) were detected in each group. According to the ABI index, the observation group was divided into three subgroups, namely, the mild group (n = 45), the moderate group (n = 42), and the severe group (n = 23). Pearson correlation analysis was used to analyze the relationship between serum CysC, IMA, and LP-PLA2 levels in patients with T2DM with LEASOD and their condition. The receiver operator characteristic (ROC) curve was used to analyze the diagnostic value of serum CysC, IMA, and LP-PLA2 levels in patients with T2DM with LEASOD.ResultsThe serum levels of CysC, IMA, and LP-PLA2 in the observation group were higher than those in the control group (p < 0.05). The serum levels of CysC, IMA, and LP-PLA2 in the severe and the moderate group were higher than those in the mild group, and the serum levels of CysC, IMA, and LP-PLA2 in the severe group were higher than those in the moderate group (p < 0.05). Pearson correlation analysis showed that CysC, IMA, and LP-PLA2 levels were all negatively correlated with ABI (r = −0.802, r = −0.757, r = −0.764, p < 0.001). The ROC curve results showed that the area under the curve (AUC) of serum CysC in the diagnosis of T2DM with LEASOD was 0.806, and the best cut-off value was 1.74 mg/L. The AUC of serum IMA for diagnosis of T2DM with LEASOD was 0.772, and the best cut-off value was 92.58 g/L. The AUC of serum LP-PLA2 in the diagnosis of T2DM with LEASOD was 0.781, and the best cut-off value was 544.86 ng/L. The AUC of the three combined diagnoses of T2DM with LEASOD was 0.863.ConclusionSerum levels of CysC, IMA, and LP-PLA2 were increased in patients with T2DM with LEASOD. Serum CysC, IMA, and LP-PLA2 are closely related to the severity of the disease. The higher the serum levels of CysC, IMA, and LP-PLA2, the more serious the degree of lower extremity arteriosclerosis occlusion, which can be used as an important serum marker to monitor the severity of T2DM with LEASOD. The combined detection of serum CysC, IMA, and LP-PLA2 has good diagnostic value for patients with T2DM with LEASOD.

<b><i>Background:</i></b> Many studies have confirmed that circular RNA (circRNA) is an important target for regulating human disease progression. This study aimed to explore the role of circ_0068087 in diabetic nephropathy (DN) progression. <b><i>Methods:</i></b> High glucose (HG)-induced renal tubular cells (HK2) were used to mimic DN cell models in vitro. The expression levels of circ_0068087, microRNA (miR)-106a-5p, and Rho-associated coiled-coil-containing kinase 2 (ROCK2) were detected by quantitative real-time PCR. Cell proliferation and apoptosis were examined by cell counting kit-8 assay, 5-ethynyl-2′-deoxyuridine assay, colony formation assay, and flow cytometry. The protein levels were examined by Western blot analysis. Cell oxidative stress was assessed by measuring MDA level and SOD activity, and cell inflammation was evaluated by detecting the concentrations of inflammatory factors. RNA interaction was verified by dual-luciferase reporter assay and RNA pull-down assay. <b><i>Results:</i></b> The present study showed that circ_0068087 was highly expressed in the serum of DN patients and HG-induced HK2 cells. Interference of circ_0068087 alleviated HG-induced apoptosis, oxidative stress, inflammation, and fibrosis in HK2 cells, while accelerated cell proliferation. miR-106a-5p could be sponged by circ_0068087, and its inhibitor eliminated the regulation of circ_0068087 knockdown on HG-induced HK2 cell injury. ROCK2 was a target of miR-106a-5p, and its expression was suppressed by circ_0068087 knockdown. miR-106a-5p overexpression suppressed HG-induced HK2 cell injury, and this effect was reversed by ROCK2 upregulation. <b><i>Conclusion:</i></b> Our data indicated that circ_0068087 downregulation mitigated HG-induced HK2 cell injury through the miR-106a-5p/ROCK2 axis, providing a potential circRNA-targeted therapy for DN.