Effect of Toll-Like Receptor 4/Myeloid Differentiation Factor 88 Inhibition by Salvianolic Acid B on Neuropathic Pain After Spinal Cord Injury in Mice

Wang, Yufeng; Xu, Xiaoqing; Hu, Peipei; Jia, Ning; Ji, Shiliang; Yuan, Haiqing

doi:10.1016/j.wneu.2019.08.086

Cited by 12 publications

(8 citation statements)

References 24 publications

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“…Some studies have found that SP can affect the IL-6 and TNF- α expression in mast cells through the NF- κ B pathway [ 36 ], whereas NF- κ B is also involved in the SP mechanism on asthma [ 37 ]. Another study found that SP can be involved in disease development through the MyD88 pathway [ 38 ]. Therefore, the lung bronchial epithelial cell line BEAS-2B was treated with different SP concentrations.…”

Section: Resultsmentioning

confidence: 99%

Bioinformatic Analysis and Cellular Assays Identify Substance P Influencing Th17/Treg Differentiation via the MyD88 Pathway as a Potential Contributor to the Progression of Asthma and Allergic Rhinitis

Liu

et al. 2022

Disease Markers

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Objective. This study is aimed at investigating the role of substance P (SP) in the development of asthma. Methods. The Gene Expression Omnibus (GEO) database was used to characterize SP expression in allergic rhinitis (AR) and asthma. Peripheral blood was collected from patients with asthma or AR. The expression of relevant cytokines and neuropeptides was measured. Enzyme-linked immunosorbent assay (ELISA) was also performed. The mast cell line LAD2 and the lung bronchial epithelial cell line BEAS-2B were treated with different concentrations of SP concentration. Then, the qRT-PCR method was used to determine the mRNA expression. Furthermore, p38 and p65 and their associated phosphorylated proteins (p-p38 and p-p65) were further validated by western blotting. Result. Clinical and GSE75011 data analysis suggested that MyD88 expression was upregulated in AR and asthma. Through the gene set variation analysis (GSVA), MyD88-related pathways were noticed and further investigated. ELISA results suggested that the SP expression was significantly increased in AR and asthma and IL-10 expression was decreased, whereas the expression of IL-6, IL-17A, IL-23, and TGF-β expressions increased. The mast cell line LAD2 was treated with different SP concentrations, and ELISA results showed that the expression of IL-6, IL-17A, IL-23, and TGF-β in the cell supernatant gradually increased with increasing SP concentrations, whereas that of IL-10 decreased. The lung bronchial epithelial cell line BEAS-2B was treated with different SP concentrations, and the expression of myeloid differentiation factor 88 (MyD88) and its related proteins was elevated. The expression of p38 and p-p38 proteins was elevated after SP treatment, and their expression levels elevated as SP concentrations increased. Finally, MyD88 expression at the single-cell level was also demonstrated. Conclusion. SP may affect the cytokine expression through the MyD88 pathway, thereby influencing Th17/Treg differentiation and eventually participating in the pathological process of asthma and AR. There are many pathological similarities between allergic rhinitis (AR) and bronchial asthma. In the present study, SP was found to possibly activate downstream inflammatory signaling pathways via MyD88, thereby affecting Th17/Treg differentiation and ultimately participating in the pathological process of asthma and AR.

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Section: Resultsmentioning

confidence: 99%

Bioinformatic Analysis and Cellular Assays Identify Substance P Influencing Th17/Treg Differentiation via the MyD88 Pathway as a Potential Contributor to the Progression of Asthma and Allergic Rhinitis

Liu

et al. 2022

Disease Markers

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“…Although there are reports between inflammation, activated microglia and SCI (J. Chen, Wang, et al, 2017; S. Xu et al, 2020), there are reports of TLR4 and chronic constrictive injury‐induced NP and peripheral NP (Jin et al, 2021; Y. Li et al, 2019); there are no studies on TLR4 expressions in microglia and SCI‐NP. A study showed that a drug named Salvianolic Acid B could inhibit the TLR4/MyD88 pathway and relieve NP after SCI (Y. Wang, Xu, et al, 2019), but it remains unknown whether TLR4 is directly related to SCI‐NP. Another study showed that morphine could increase the expressions of TLR4 in the spinal cord to amplify mechanical allodynia (Ellis et al, 2016), but it is not yet clear whether inhibiting TLR4 can release SCI‐NP and whether TLR4 is directly related to NP.…”

Section: Discussionmentioning

confidence: 99%

“…A study showed that a drug named Salvianolic Acid B could inhibit the TLR4/MyD88 pathway and relieve NP after SCI (Y. Wang, Xu, et al, 2019), but it remains unknown whether TLR4 is directly related to SCI-NP. Another study showed that morphine could increase the expressions of TLR4 in the spinal cord to amplify mechanical allodynia (Ellis et al, 2016), but it is not yet clear whether inhibiting TLR4 can release SCI-NP and whether TLR4 is directly related to NP.…”

Section: Discussionmentioning

confidence: 99%

Systematic analysis of critical genes and pathways identified a signature of neuropathic pain after spinal cord injury

Bai

Zhang

et al. 2022

Eur J of Neuroscience

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Spinal cord injury (SCI) damages sensory systems, producing chronic neuropathic pain that is resistant to medical treatment. The specific mechanisms underlying SCI-induced neuropathic pain (SCI-NP) remain unclear, and protein biomarkers have not yet been integrated into diagnostic screening. To better understand the host molecular pathways involved in SCI-NP, we used the bioinformatics method, the PubMed database and bioinformatics methods to identify target genes and their associated pathways. We reviewed 2504 articles

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“…We chose Sm4CL2 to build two combinations, Sm4CL2-SmRAS and Sm4CL2-CbRAS, resulting in two engineered yeast strains YW-24 and YW-25, respectively, considering our previous finding that Sm4CL2 originating from S. miltiorrhiza has high PA and CA utilization efficiency. 34 When 180.0 mg/L (1 mM) of CA (3) and 198.0 mg/L (1 mM) of DHPL ( 6) were added as substrates, YW-24 and YW-25, respectively, yielded 43.5 ± 2.4 and 29.0 ± 2.6 mg/L of RA (7) after 72 h of incubation (Figure 3B), which proved that CA (3) could be activated to CA-CoA and that Sm4CL2-SmRAS had higher substrate conversion efficiency than Sm4CL2-CbRAS did; thus, the Sm4CL2-SmRAS module was selected for further study.…”

Section: ■ Resultsmentioning

confidence: 99%

“…Salvianolic acid B (SAB), also called lithospermic acid B, is a plant-derived natural product with a wide range of associated biological activities, including antioxidant, anti-inflammatory, , immunomodulatory, and anti-liver fibrosis, against liver injury , and neuroprotection effects. , This compound has been clinically used to treat cardio- and cerebrovascular diseases and also has great potential as a health care product and medicine for the treatment of other disorders. − It has been proved that SAB could eliminate chronic mild stress-induced depression through suppressing oxidative stress and neuroinflammation, regulate gut microbiota abundances and LPS/TLR4 signaling pathway in obese mice and block CD36 to counteract JUN-mediated fibrosis efficacy in both human fibroblasts and mouse wounds, which makes SAB a potential health-promoting food and therapeutic agent against depression, obesity, and pathologic skin scarring. At the clinic, the salvianolic acids for injection, of which SAB accounts for 63.2%, combined with conventional treatment of acute cerebral infarction could improve the total effective rate, neurological deficit, and ability to perform activities of daily living .…”

Section: Introductionmentioning

confidence: 99%

De novo Biosynthesis of Salvianolic Acid B in Saccharomyces cerevisiae Engineered with the Rosmarinic Acid Biosynthetic Pathway

Geng

Zhang

et al. 2022

J. Agric. Food Chem.

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Salvianolic acid B (SAB), also named lithospermic acid B, belongs to a class of water-soluble phenolic acids, originating from plants such as Salvia miltiorrhiza. SAB exhibits a variety of biological activities and has been clinically used to treat cardio- and cerebrovascular diseases and also has great potential as a health care product and medicine for other disorders. However, its biosynthetic pathway has not been completely elucidated. Here, we report the de novo biosynthesis of SAB in Saccharomyces cerevisiae engineered with the heterologous rosmarinic acid (RA) biosynthetic pathway. The created pathway contains seven genes divided into three modules on separate plasmids, pRS424-FjTAL-Sm4CL2, pRS425-SmTAT-SmHPPR or pRS425-SmTAT-CbHPPR, and pRS426-SmRAS-CbCYP-CbCPR. These three modules were cotransformed into S. cerevisiae, resulting in the recombinant strains YW-44 and YW-45. Incubation of the recombinant strains in a basic medium without supplementing any substrates yielded 34 and 30 μg/L of SAB. The findings in this study indicate that the created heterologous RA pathway cooperates with the native metabolism of S. cerevisiae to enable the de novo biosynthesis of SAB. This provides a novel insight into a biosynthesis mechanism of SAB and also lays the foundation for the production of SAB using microbial cell factories.

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Effect of Toll-Like Receptor 4/Myeloid Differentiation Factor 88 Inhibition by Salvianolic Acid B on Neuropathic Pain After Spinal Cord Injury in Mice

Cited by 12 publications

References 24 publications

Bioinformatic Analysis and Cellular Assays Identify Substance P Influencing Th17/Treg Differentiation via the MyD88 Pathway as a Potential Contributor to the Progression of Asthma and Allergic Rhinitis

Bioinformatic Analysis and Cellular Assays Identify Substance P Influencing Th17/Treg Differentiation via the MyD88 Pathway as a Potential Contributor to the Progression of Asthma and Allergic Rhinitis

Systematic analysis of critical genes and pathways identified a signature of neuropathic pain after spinal cord injury

De novo Biosynthesis of Salvianolic Acid B in Saccharomyces cerevisiae Engineered with the Rosmarinic Acid Biosynthetic Pathway

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