Effectiveness of Bailing capsules in the treatment of lupus nephritis: A meta­analysis.

Previous studies have explored the treatment of lupus nephritis with Bailing capsules; however, due to limited sample sizes and inconsistent results across these studies, no definitive conclusions have been drawn. Thus, the present study aimed to provide evidence for the effectiveness of Bailing capsules in the treatment of lupus nephritis. To obtain relevant clinical studies (published before 20 July 2019), PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure, WanFang and the Chinese Biomedical Literature Database were searched, and relevant studies concerning the use of Bailing capsules for treating lupus nephritis were selected. The extracted data were general characteristics such as the first author, publication year, study year, follow­up time, age, sex, course of the disease and a number of outcome indicators. These included systemic lupus erythematosus disease activity index (SLEDAI) score, serum albumin (Alb), 24­h urinary protein, serum creatinine, anti­ds­DNAIgM, complement component 3 (C3), and the number of effective treatments and complications. Meta­analysis was performed using R­3.12 software. Publication bias was assessed using Egger's test. A total of 14 studies comprising 1,301 participants were combined for analysis in the present study. The results demonstrated that with the exception of anti­ds­DNAIgM and complement C3, other indicators, such as SLEDAI score, Alb, 24­h urinary protein, serum creatinine, and the number of effective treatments and complications) in the Bailing capsule treatment group were improved compared with those in the control group. The results of the present meta­analysis suggested that Bailing capsules may be effective in the treatment of lupus nephritis.

Sclerostin/Receptor Related Protein 4 and Ginkgo Biloba Extract Alleviates ß-Glycerophosphate-Induced Vascular Smooth Muscle Cell Calcification By Inhibiting Wnt/ß-Catenin Pathway.

BACKGROUND: Abnormal mineral metabolism in patients with chronic kidney disease (CKD) may lead to vascular calcification, which is markedly associated with adverse events, including ischemic cardiac diseases and all-cause cardiovascular mortality. Thus, preventing and treating vascular calcification play an important role in improving the prognosis of CKD patients. OBJECTIVES: To investigate the potential functions of sclerostin and low-density lipoprotein receptor-related protein 4 (Lrp4) in alleviating the ß-glycerophosphate (ß-GP)-induced vascular smooth muscle cell (VSMC) calcification, and the protective effect of Ginkgo biloba extract (GBE). METHODS: VSMC were extracted from Sprague-Dawley rat aorta and cultured in medium. The VSMCs were divided into 3 groups: (1) Negative control group, (2) ß-GP group, in which the VSMCs were treated with ß-GP, and (3) GBE and ß-GP group, where the VSMCs were treated with both ß-GP and GBE. The calcium nodules within the cells were examined by using Alizarin red S staining. The mRNA expression levels of ß-catenin and bone gamma-carboxyglutamic-acid-containing proteins (BGP) were detected by real-time PCR. The protein levels of sclerostin and Lrp4 were determined by Western blot. RESULTS: Alizarin red S staining showed that the VSMCs in ß-GP group had a distinct orange-red precipitate when compared with VSMCs in the negative control group, while the orange-red precipitate of the GBE and ß-GP group was significantly reduced compared to the ß-GP group. Real-time PCR showed that the mRNA levels of ß-catenin and BGP in VSMCs of ß-GP group were significantly higher than those of the negative control group (p < 0.05); while they were significantly reduced in VSMCs of the GBE and ß-GP group (p < 0.05). Western blot results showed that the expression of sclerostin in the ß-GP group was significantly higher than that in the control group (p < 0.05), whereas Lrp4 was significantly lower than in control group (p < 0.05). Sclerostin in GBE and ß-GP group was significantly reduced (p < 0.05), but Lrp4 was significantly elevated when compared with that of the ß-GP group (p < 0.05). CONCLUSION: ß-GP induced VSMC calcification by activating the Wnt/ß-catenin signaling pathway. Sclerostin and Lrp4 were involved in ß-GP-induced VSMC calcification and play an important role. GBE could alleviate VSMC calcification induced by ß-GP through inhibiting the Wnt/ß-catenin signaling pathway.