Objective. To elucidate the main mechanism of Xijiao Dihuang decoction (XJDHT) for the treatment of systemic lupus erythematosus (SLE). Methods. TCMSP, BATMAN-TCM, ETCM, and TCMID databases and literature search were used to screen the potential active compounds of XJDHT, and TCMSP and SwissProt databases were searched to predict the targets of the compounds. The targets of SLE were obtained from Genegards, OMIM, and DisGeNET databases, and Venn online platform was used to obtain the intersection targets of XJDHT and SLE. Afterwards, the PPI network was constructed by using the STRING database, and the core targets were identified by network topology analysis. GO and KEGG enrichment analyses were performed through R software, and molecular docking of the top three core targets and their corresponding compounds were accomplished by Autodock Vina and Pymol softwares. Results. There were 30 potential active ingredients, 289 potential targets, and 129 intersection targets screened from the above databases. Network topology analysis identified 23 core targets, such as AKT1, TNF, IL6, IL1B, and INS. GO enrichment analysis obtained 2555 terms and mainly clustering on the react to lipopolysaccharide, membrane raft, and ubiquitin-like protein ligase binding. KEGG enrichment analysis obtained 187 signaling pathways, mainly concentrating on the lipid and atherosclerosis, AGE-RAGE signaling pathway in diabetic complications, fluid shear stress, and atherosclerosis. Molecular docking verified that the active compounds of XJDHT have the strong binding activity to the core targets. Conclusion. This study preliminarily uncovers the mechanism of XJDHT acting on SLE through a “multicompound, multitarget, and multipathway” manner. XJDHT may achieve the treatment of SLE by inhibiting the proinflammatory factors, inflammatory signal cvtokines, proliferation, injury, and apoptosis processes. In summary, the present study would provide a promising theoretical basis for further clinical and experimental studies.

Interleukin- (IL-) 33 contributes to various inflammatory processes. IL-33/ST2 activation participates in systemic lupus erythematous via binding to the receptor of Suppression of Tumorigenicity 2 protein (ST2). However, whether IL-33/ST2 interferes with the nosogenesis of cutaneous lupus erythematosus (CLE) has not been reported so far. Herein, we proposed to disclose the impacts on IL-33/ST2 activation and Ro60 on CLE and their potential implications in the photosensitization of CLE cells. IL-33, ST2, and Ro60 in CLE patients’ skin lesions were detected. Murine keratinocytes stimulated with or without IL-33 were irradiated by ultraviolet B (UVB), and the levels of Ro60 and inflammation markers were determined. Keratinocytes were cocultured with J774.2 macrophages and stimulated with IL-33 for analysis of chemostasis. The results identified that IL-33, ST2, and downstream inflammation markers were significantly upregulated in CLE lesions with Ro60 overexpression. Additionally, IL-33 treatment promoted the upregulation of Ro60 induced by UVB treatment in murine keratinocytes. Moreover, IL-33 stimulates keratinocytes to induce macrophage migration via enhancing the generation of the chemokine (C–C motif) ligands 17 and 22. Meanwhile, the silencing of ST2 or nuclear factor-kappa B (NF-κB) suppression abolished IL-33-induced upregulation of Ro60 in keratinocytes. Similarly, the inhibition of SOX17 expression was followed by downregulation of Ro60 in keratinocytes following IL-33 stimulation. In addition, UVB irradiation upregulated SOX17 in keratinocytes. Conclusively, the IL-33/ST2 axis interferes with Ro60-regulated photosensitization via activating the NF-κB- and PI3K/Akt- and SOX17-related pathways.

Objective: To analyze the characteristics of pulse pattern parameters of systemic lupus erythematosus (SLE) patients and the factors influencing their TCM patterns, and to provide an objective basis for their TCM pulse diagnosis and diagnosis. Methods: The SmartTCM-A1 TCM intelligent detection system was used to collect pulse diagnosis image information from 267 SLE patients (140 in the Yin deficiency internal heat evidence group, 96 in the heat toxin incandescence evidence group, and 31 in the rheumatic heat paralysis evidence group) and 130 healthy individuals, extract the image parameters of pulse diagnosis, and analyze the characteristics of pulse diagnosis parameters of SLE patients and their influencing factors of pulse diagnosis parameters of different TCM evidence types by logistic regression model. Results: ① Compared with the healthy group, the pulse parameters h1 value, h4 value, and t1/t value were significantly higher in the SLE group (P<0.05) and the pulse parameter t value was significantly lower in the SLE group (P<0.05); logistic regression analysis showed that the independent influencing factors in SLE patients included: h4 value (OR=1.073; 95% CI=1.003-1.148 ;P<0.05), t-value (OR=0.003;95% CI=0.000-0.763;P<0.05) and t1/t-value (OR=0.000;95% CI=0.000-1.199;P<0.05). ② Compared with the group with incandescent heat toxin evidence, the h4 value, h5 value, t4 value, t5 value, t5/t4 value were significantly lower in the group with Yin deficiency internal heat evidence (P<0.05), the h4/h1 value and t1/t4 value were significantly higher in the group with Yin deficiency internal heat evidence (P<0.05), the h4 value, h5 value, t5 value, h4/h1 value were significantly lower in the group with rheumatic heat paralysis evidence (P<0.05), and the t4 value, h5/h1 value, t5/t1 value were significantly lower in the group with rheumatic heat paralysis evidence (P<0.05). , h5/h1 values, and t1/t4 values were significantly higher in the rheumatism-heat paralysis group (P<0.05); logistic regression analysis. The results showed that the independent influencing factors of TCM evidence in SLE patients included: h3 values in the yin deficiency internal heat evidence group (OR=2.295; 95% CI=1.843-2.858; P<0.05) and h3 values in the rheumatic heat paralysis evidence group (OR=2.309; 95% CI=1.87-2.85; P<0.05). Conclusion:. Conclusion Pulse diagnosis parameters h4 value, t value and t1/t value are one of the influencing factors for the diagnosis of SLE patients, and pulse diagnosis parameter h3 value is one of the influencing factors for the diagnosis of SLE Chinese medical evidence.

Objective. From the pathogenic mechanism point of view, systemic lupus erythematosus (SLE) features prominently in T lymphocyte apoptosis. Yet the regulatory mechanism underlying SLE cell apoptosis remains to be explored. This research intends to clarify the role played by miR-137 in SLE and the underlying mechanisms. Methods. Twenty SLE patients (SLE group) and twenty healthy controls (control group) were selected, from whom peripheral blood CD4+ T cells were isolated via magnetic-activated cell sorting. Reverse transcription-polymerase chain reaction (RT-PCR) quantified miR-137 and AMP-activated protein kinase (AMPK) in CD4+ T cells. Further, transfection of miR-137 mimics and inhibitors into CD4+ T cells was carried out to alter miR levels. Levels of pyroptosis, apoptosis, and inflammatory- and pyroptosis-related proteins were determined through PI staining, flow cytometry, and Western blotting, respectively. A luciferase reporter gene assay identified the targeting relation between miR-137 and AMPK. Results. SLE patients showed downregulated miR-137 and upregulated AMPK in CD4+ T cells than controls. miR-137 upregulation by miR-137 mimic transfection inhibited Jurkat cell pyroptosis and apoptosis at both mRNA and protein levels and suppressed NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome activity and pyroptosis-related protein gasdermin D (GSDMD), while miR-137 inhibitor transfection contributed to completely opposite effects. miR-137 directly targeted AMPK, as indicated by the luciferase reporter gene assay. Furthermore, miR-137 inhibitor intervention induced healthy CD4+ T cell pyroptosis and apoptosis via mediating AMPK, whereas miR-137 mimic transfection into CD4+ T cells of SLE patients leads to opposite results. Conclusion. Upregulating miR-137 inhibits CD4+ T cell pyroptosis in SLE patients by modulating the AMPK pathway, suggesting the potential diagnostic and therapeutic role of miR-137 in SLE.

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