Therapeutic effect of total saponins from Dioscorea nipponica makino on gouty arthritis based on the NF-κB signal pathway: An In vitro study

Zhou, Qi; Liu, Shumin; Yua, Donghua; Zhang, Ning

doi:10.4103/0973-1296.186344

Cited by 12 publications

(1 citation statement)

References 18 publications

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“…Total saponins from Dioscorea nipponica Makino are the principal components that show antiinflammatory effects. 13,16 Our previous study showed that the content of TDN was 55%, and the UPLC-MS method was used to verify that its main components were dioscin, protodioscin, and pseudo protodioscin. The MTT method was also used to test the active component of TDN.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Effects of Total Saponins From Dioscorea nipponica Makino on Gouty Arthritis Based on the MAPK-PPARγ Signaling Pathway: An In Vitro Study

Zhou

Zhang

et al. 2020

Natural Product Communications

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Gouty arthritis (GA) is an inflammatory disease caused by the deposition of monosodium urate in the synovial membrane and cartilage due to a high concentration of uric acid in the blood. Dioscorea nipponica Makino is widely used in the clinic to treat GA. Total saponins are its main components and showed an anti-inflammatory effect on GA in a previous study. The mitogen-activated protein kinase (MAPK)-peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway plays a key role during the onset of GA; however, little is known about its potential mechanism. Based on in vitro experiments, this study aims to determine the mechanism of total saponins from Dioscorea nipponica Makino (TDN) in treating GA by regulating the MAPK-PPARγ signaling pathway. Fibroblast-like synoviocytes were divided into 3 groups: the model group, which was given 10 µg/L IL-1β to induce proliferation; TDN group (10 µg/L IL-1β + 100 µg/L TDN); and indomethacin group (10 µg/L IL-1β + 100 µg/L indomethacin). Seventy-two hours after treatment, the real-time PCR method was used to detect the mRNA expression levels of extracellular signal regulated kinase 1/2 (ERK1/2), p-38, c-Jun N-terminal kinase (JNK), IKKα, c-Jun, MAPK phosphatase (MKP), vascular cell adhesion molecule 1 (VCAM1), intercellular adhesion molecule 1 (ICAM1), C-X-C motif chemokine ligand 1 (CXCL1), PPARγ, and Adipor2. The Western blot method was used to detect the protein expression of ERK1/2, p-ERK1/2, p-38, p-P38, JNK, p-JNK, IKKα, p-IKKα, c-Jun, p-c-Jun, MKP, p-MKP, VCAM1, ICAM1, CXCL1, PPARγ, and Adipor2. Compared with the model group, the TDN group displayed significantly increased mRNA expression of c-Jun, MKP, CXCL1, PPARγ, and Adipor2 and significantly decreased mRNA expression of ICAM1. Compared with the model group, the TDN group exhibited significantly increased protein expression of MKP and significantly decreased protein expression of p-ERK1/2, p-38, p-JNK, p-IKKα, p-c-Jun, VCAM1, ICAM1, and PPARγ. Our results indicated that TDN could treat GA by influencing the MAPK-PPARγ signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Therapeutic Effects of Total Saponins From Dioscorea nipponica Makino on Gouty Arthritis Based on the MAPK-PPARγ Signaling Pathway: An In Vitro Study

Zhou

Zhang

et al. 2020

Natural Product Communications

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Integrative metabolomics and network pharmacology to study the preventative impact of dioscin treatment on hyperuricemia

Wang

et al. 2023

Biomedical Chromatography

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This work aims to combine network pharmacology and metabolomics to explore the mechanism of action of dioscin on hyperuricemia (HUA). The preventative impact of dioscin on HUA and its putative mechanism were examined using network pharmacological analysis and metabonomics. Network pharmacology study further pointed out the potential targets of dioscin after a review of the relevant biomarker pathways discovered by metabolomic analysis. Molecular docking was then used to examine how the active chemicals interacted with the target proteins. The therapeutic effect of dioscin on HUA was shown to be mediated by 13 potentially important metabolites as a result of metabonomic research. Most of these metabolites are regulated after dioscin therapy to help patients recover. Based on network pharmacology, we identified 10 central genes, which is partly in agreement with metabolomics data. Using metabolomics and network pharmacology, this study investigated the primary targets and mechanisms of dioscin in the treatment of HUA. It is advantageous that dioscin has been developed as an additional drug for the treatment of HUA.

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Dioscin ameliorates inflammatory bowel disease by up‐regulating miR‐125a‐5p to regulate macrophage polarization

Shi

Zhang

Jin

et al. 2022

Clinical Laboratory Analysis

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Purpose Dioscin has been proven to have anti‐cancer, anti‐inflammatory, and anti‐infection roles. However, the role of Dioscin in inflammatory bowel disease (IBD) and its related mechanisms is unclear and needs further study. Methods The colitis model in mice was established. After Dioscin (20, 40, or 80 mg/kg) treatment, the colon length was measured by a ruler. Histopathology, inflammatory cytokines, gut permeability, tight junction proteins, macrophage infiltration, macrophage polarization, and miR‐125a‐5p level were detected by hematoxylin–eosin staining, enzyme‐linked immunosorbent assay, quantitative real‐time polymerase chain reaction (qRT‐PCR), FITC‐dextran, Western blot, and flow cytometry. In vitro experiments, after RAW264.7 cells induced by lipopolysaccharide (LPS)/interleukin‐4 (IL‐4), were treated with Dioscin and miR‐125a‐5p inhibitor, miR‐125a‐5p level, cell vitality, inflammatory cytokines, and M1/M2 marker genes were measured by qRT‐PCR and MTT assay. Results Dioscin (20, 40, or 80 mg/kg) relieved DSS‐triggered colitis and restrained the serum and colon of pro‐inflammatory cytokines expression. Meanwhile, different concentrations' Dioscin weakened M1 macrophage polarization but facilitated tight junction protein expressions, M2 macrophage polarization, and miR‐125a‐5p level in colitic mice. Moreover, miR‐125a‐5p inhibitor reversed the modulation of Dioscin on miR‐125a‐5p expression, cell vitality, and inflammatory cytokines in lipopolysaccharide (LPS)‐induced RAW264.7 cells. We further discovered that Dioscin restrained M1 marker gene (CD16) expression while intensifying M2 marker genes (CD206 and Arginase‐1) expressions in vitro , which was reversed by miR‐125a‐5p inhibitor. Conclusion Dioscin modulated macrophage polarization by increasing miR‐125a‐5p, thereby improving the intestinal epithelial barrier function and reducing IBD.

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Therapeutic effect of total saponins from Dioscorea nipponica makino on gouty arthritis based on the NF-κB signal pathway: An In vitro study

Cited by 12 publications

References 18 publications

Therapeutic Effects of Total Saponins From Dioscorea nipponica Makino on Gouty Arthritis Based on the MAPK-PPARγ Signaling Pathway: An In Vitro Study

Therapeutic Effects of Total Saponins From Dioscorea nipponica Makino on Gouty Arthritis Based on the MAPK-PPARγ Signaling Pathway: An In Vitro Study

Integrative metabolomics and network pharmacology to study the preventative impact of dioscin treatment on hyperuricemia

Dioscin ameliorates inflammatory bowel disease by up‐regulating miR‐125a‐5p to regulate macrophage polarization

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