Lupus nephritis (LN) is one of the most common clinical manifestations of systemic lupus erythematosus (SLE), causing death and disability. The current research study explored whether there was any improvement effect on LN after emodin administration. Network pharmacology was used to screen the target genes of emodin for the treatment of LN. LPS and IL-4 were employed for RAW264.7 macrophage M1/M2 polarization induction, and 0.1% HgCl2 was used for the LN rat model’s establishment. Flow cytometry was performed to detect the effect of 20, 40, and 80 µM emodin on RAW264.7 macrophage polarization. HE and PAS staining were subsequently conducted to detect 70 mg/kg emodin action on renal injury in LN rats. The effect of emodin on the content of urinary proteins and dsDNA antibodies was also determined. The results indicated that peroxisome proliferators-activated receptors gamma (PPARG) may be a target gene of emodin in LN, and emodin had no significant toxicity to macrophages at different concentrations. Compared with the control, emodin significantly inhibited LPS-induced polarization in M1 macrophages and improved that of IL-4-induced M2 macrophages. Besides, emodin alleviated kidney injury and markedly reduced the levels of urinary protein and dsDNA antibodies in rats. Moreover, after targeting interference with the PPARG expression, the improvement effect of emodin on LN is significantly reduced, indicating that emodin may relieve the symptoms of LN by activating the PPARG expression. Our study revealed that PPARG may be applied as a new therapy for LN.

Background. Diabetic microvascular complications are the main causes of organ dysfunction and even death in diabetic patients. Our previous studies confirmed the beneficial effects of Yiqi Jiedu Huayu Decoction (YJHD) on diabetic cardiomyopathy and diabetic nephropathy. It is not clear whether YJHD can treat multiple diabetic microvascular complications including diabetic retinopathy, diabetic cardiomyopathy, and diabetic nephropathy through some common mechanisms. Methods. TCMSP, SymMap, STITCH, Swiss Target Prediction, and SEA databases were used to collect and analyze the components and targets of YJHD. GeneCards, DrugBank, DisGeNET, OMIM, and GEO databases were used to obtain target genes for diabetic retinopathy, diabetic cardiomyopathy, and diabetic nephropathy. The GO and KEGG enrichment analyses were performed on the DAVID and STRING platforms. Molecular docking was used to evaluate the binding sites and affinities of compounds and target proteins. Animal experiments were designed to validate the network pharmacology results. Results. Through network pharmacological analysis, oxidative stress, inflammatory response, and apoptosis were identified as key pathological phenotypes for the treatment of diabetic microvascular complications with YJHD. In addition, JNK, p38, and ERK1/2 were predicted as key targets of YJHD in regulating the abovementioned pathological phenotypes. The results of animal experiments showed that YJHD could ameliorate retinal pathological changes of diabetes rats. YJHD can inhibit oxidative stress and inflammation in heart and kidney of diabetic rats. Molecular docking showed strong binding between compounds and JNK, p38, and ERK1/2. Berlambine may play a key role in the treatment process and is considered as a promising regulator of MAPK protein family. The regulatory effects of YJHD on JNK, p38, and ERK1/2 were demonstrated in animal experiments. Conclusions. YJHD may play a therapeutic role in diabetic microvascular complications by regulating oxidative stress, inflammatory response, and apoptosis. The regulation of JNK, p38, and ERK1/2 phosphorylation may be the key to its therapeutic effect.

Background. Renal epithelium lesions can cause renal cell carcinoma. This kind of tumor is common among all renal cancers with poor prognosis, of which more than 70% belong to kidney renal clear cell carcinoma. As the pathogenesis of KIRC has not been elucidated, it is necessary to be further explored. Methods. The Genomic Spatial Event database was used to obtain the analysis dataset (GSE126964) based on the GEO database, and The Cancer Genome Atlas was applied for KIRC data collection. edgeR and limma analyses were subsequently conducted to identify differentially expressed genes. Based on the systems biology approach of WGCNA, potential biomarkers and therapeutic targets of this disease were screened after the establishment of a gene coexpression network. GO and KEGG enrichment used cluster Profiler, enrichplot, and ggplot2 in the R software package. Protein-protein interaction network diagrams were plotted for hub gene collection via the STRING platform and Cytoscape software. Hub genes associated with overall survival time of KIRC patients were ultimately identified using the Kaplan-Meier plotter. Results. There were 1863 DEGs identified in total and ten coexpressed gene modules discovered using a WGCNA method. GO and KEGG analysis findings revealed that the most enrichment pathways included Notch binding, cell migration, cell cycle, cell senescence, apoptosis, focal adhesions, and autophagosomes. Twenty-seven hub genes were identified, among which FLT1, HNRNPU, ATP6V0D2, ATP6V1A, and ATP6V1H were positively correlated with OS rates of KIRC patients ( p < 0.05 ). Conclusions. In conclusion, bioinformatic techniques can be useful tools for predicting the progression of KIRC. DEGs are present in both KIRC and normal kidney tissues, which can be considered the KIRC biomarkers.