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Additional file 2. Table S1. The information of siRNA and primer sequences used in this study. Table S2. The information of antibodies used in this study. Table S3. E xpression patterns of 100 di fferentially expressed genes in SC between the sham and CCI model groups by Microarray Profiling (mixed sample, n = 3). Table S4. Expression patterns of 100 differentially expressed genes in SC between the sham and CCI model groups by RNA-seq (n = 4).

Additional file 1. Figure S1. Clec7a knockdown alleviated LPS and ATP induced BV2 cells pyroptosis. Figure S2. C/EBP β knockdown alleviated LPS and ATP induced BV2 cells pyroptosis.

Additional file 6: Table S2. Quantification analysis of calcium in Gypsum Fibrosum and full prescription BHGZD by ICP-AES.

Additional file 2: Figure S2. The chromatograms of mixed standards and serum sample after BHGZD gavage.

Additional file 1: Figure S1. The chemical structure and corresponding mass spectrum of absorbed components in vivo.

Additional file 3: Figure S3. The chromatogram of selectivity of the analytes in rat serum.

Additional file 5: Table S1. Identification of chemical profile of BHGZD in vitro by UFLC-Q-TOF-MS/MS.

Additional file 1: Table S1. Includes detailed information of all enzyme-linked immunosorbent assay kits. Table S2. Includes 672 putative target genes of CRT predicted using ETCM database and TCMIP v2.0 platform. Table S3. Includes 3472 DKD-related genes from Human Phenotype Ontology (HPO), DisGeNet and Drugbank databases. Table S4. Includes enrichment results of clinical symptoms of 390 CRT putative targets. Table S5. Includes enrichment results of functional modules of 390 CRT putative targets. Table S6. Includes 231 candidate targets of CRT against DKD in ���Disease Gene-Drug Target��� interaction networks based on calculated network topological features. Table S7. Includes enrichment results of functional modules of 231 CRT candidate targets.

Additional file 4: Figure S4. Graphical abstract.

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Few data are available from prospective trials to define the hepatotoxicity of diclofenac, the most widely prescribed non-steroidal anti-inflammatory drug (NSAID) in the world. We determined the rate of laboratory and clinical adverse hepatic effects in a large double-blind trial of diclofenac.Patientsor = 50 years with rheumatoid arthritis or osteoarthritis were randomly assigned to diclofenac (150 mg daily) or etoricoxib (60 or 90 mg daily). Patients with hepatic disease or who reportedor = 14 alcoholic drinks weekly were excluded. Patients had visits (with liver tests) every 4 months and were contacted by phone between visits and every 6 months after discontinuation until the end of the study. Causality assessment was performed for liver-related hospitalizations, Hy's cases (serious adverse events with AST or ALT3 x upper limit of normal (ULN) and bilirubin2 xULN), and liver failure/transplant/death.A total of 17,289 patients received diclofenac for a mean of 18 months. Liver end points with diclofenac were ALT/AST3 xULN: 527(3.1%); ALT/AST10 xULN: 86(0.5%); liver-related hospitalizations: 4(0.023%); Hy's cases: 2(0.012%); liver failure/death/transplant: 0. Aminotransferase elevations occurred primarily within the first 4-6 months of therapy, whereas liver-related hospitalizations occurred between 9 days and 21 months.Diclofenac is commonly associated with aminotransferase elevations, generally in the first 4-6 months of therapy. Clinical liver events requiring hospitalization are relatively rare (23/100,000 patients), but may develop early or late in therapy. The markedly increased rate of aminotransferase elevation with diclofenac may not be paralleled by a proportional marked increase in clinical liver events, although clinical events potentially also may be decreased with regular monitoring in a clinical trial setting.