Sparstolonin B inhibits lipopolysaccharide-induced inflammation in 3T3-L1 adipocytes

Wang, Ming; Xiu, Liangchang; Diao, Jiang; Wei, Lianbo; Sun, Jia

doi:10.1016/j.ejphar.2015.10.050

Cited by 29 publications

(24 citation statements)

References 26 publications

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“…The latter two experiments were performed on mice [ 80 ]. Inhibition of LPS-induced inflammation in 3T3-L1 adipocytes [ 81 ] and human umbilical vein endothelial cells was also observed [ 82 ].…”

Section: Tlr4 Antagonists From Natural Sourcesmentioning

confidence: 99%

TLR4 Signaling Pathway Modulators as Potential Therapeutics in Inflammation and Sepsis

et al. 2017

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Toll-Like Receptor 4 (TLR4) signal pathway plays an important role in initiating the innate immune response and its activation by bacterial endotoxin is responsible for chronic and acute inflammatory disorders that are becoming more and more frequent in developed countries. Modulation of the TLR4 pathway is a potential strategy to specifically target these pathologies. Among the diseases caused by TLR4 abnormal activation by bacterial endotoxin, sepsis is the most dangerous one because it is a life-threatening acute system inflammatory condition that still lacks specific pharmacological treatment. Here, we review molecules at a preclinical or clinical phase of development, that are active in inhibiting the TLR4-MyD88 and TLR4-TRIF pathways in animal models. These are low-molecular weight compounds of natural and synthetic origin that can be considered leads for drug development. The results of in vivo studies in the sepsis model and the mechanisms of action of drug leads are presented and critically discussed, evidencing the differences in treatment results from rodents to humans.

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Section: Tlr4 Antagonists From Natural Sourcesmentioning

confidence: 99%

TLR4 Signaling Pathway Modulators as Potential Therapeutics in Inflammation and Sepsis

et al. 2017

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“…TLRs belong to a highly conservative pattern recognition receptor family, and are widely distributed on the surface of macrophages, monocytes, dendritic cells, natural killer cells and lymphocytes (32). The TLR family includes ≥12 members, including TLR4 (33). TLR4 has been extensively studied due to its involvement in and mediation of inflammatory reactions (34).…”

Section: Discussionmentioning

confidence: 99%

“…These proteins may enter the circulation through the injured blood brain barrier to mediate systemic inflammatory responses and lead to SCI (40). Wang et al (33) suggested that sparstolonin B may decreased high fat diet-induced obesity in rats and inhibit lipopolysaccharide-induced cytokine production via TLR4 and NF-κB expression in 3T3-L1 adipocytes. The results of the present study demonstrated that sparstolonin B markedly suppressed TLR4, MyD88 and NF-κB protein expression in SCI tissues.…”

Section: Discussionmentioning

confidence: 99%

Sparstolonin B attenuates spinal cord injury‑induced inflammation in rats by modulating TLR4‑trafficking

Yuan¹,

Zhang²,

Zhu³

et al. 2018

Mol Med Report

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The present study used a spinal cord injury (SCI) model to evaluate whether sparstolonin B was able to prevent SCI, and to investigate the underlying signaling mechanism. Sparstolonin B attenuated the SCI‑induced Batto, Beattie and Bresnahan score and water content in rats. Sparstolonin B attenuated the mRNA expression of proinflammatory cytokines interleukin (IL)‑18, IL‑6, IL‑1β, and IL‑23, decreased the levels of tumor necrosis factor‑α and interferon‑γ, and decreased caspase‑3 activity and apoptosis regulator Bax protein expression in SCI rats. Similarly, sparstolonin B inhibited monocyte chemoattractant protein‑1 mRNA levels, and Toll‑like receptor (TLR) 4, myeloid differentiation primary response protein MyD88 (MyD88) and nuclear factor (NF)‑κB protein levels in SCI rats. The present results suggested that sparstolonin B may attenuate SCI‑induced inflammation and apoptosis in rats by modulating the TLR4/MyD88/NF‑κB signaling pathway.

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“…Most strikingly, this peculiar format to report cell viability data can be found as Figure 1 even in a vast array of manuscripts that focus on the anti-inflammatory properties of specific compounds on LPS-induced inflammation in several unrelated cell models, such as mammary epithelial cells [23], 3T3-L1 adipocytes [24], BV2 microglial cells [25,26], RAW264.7 cells [27]-where it tends to constitute Figure 2, however-and umbilical vein endothelial cells [28]. This same model for Figure 1 is also found in two works on the testing of anti-inflammatory properties of different compounds on IL-1α -induced inflammation in chondrocytes [29,30].…”

Section: Figurementioning

confidence: 99%

Between Innovation and Standardization, Is There Still a Room for Scientific Reports? The Rise of a Formatting Tradition in Periodontal Research

et al. 2019

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Everybody, regardless of their role, is aware that biomedical research is rapidly evolving, and the demand for reproducibility is increasing together with the amount of novel information. “Before reproducibility must come pre-producibility” “Checklists work to improve science”, just to quote some of the articles querying how to find a new bridge between ethics in science and the urgency for publishing. Looking for papers on anti-inflammatory compounds in periodontics, we came across a significant number of articles that could be considered a prototype of a consistent study format. The literature on the testing of active compounds on lipopolysaccharides- (LPS)-induced inflammation in gingival fibroblasts was searched to identify studies that followed a consistent format, to better understand their similarities and assess the appropriateness of their methods. Several studies were identified with a degree of similarity in their methods and formatting that was so high that it was possible to rule out that it was due to chance, and a format template common to these studies was outlined. Although this was most likely beyond the intentions of their authors, these studies may pose the basis for an in-vitro testing standard for anti-inflammatory compounds; however, the dangers of acritical uniformity are also apparent.

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Sparstolonin B inhibits lipopolysaccharide-induced inflammation in 3T3-L1 adipocytes

Cited by 29 publications

References 26 publications

TLR4 Signaling Pathway Modulators as Potential Therapeutics in Inflammation and Sepsis

TLR4 Signaling Pathway Modulators as Potential Therapeutics in Inflammation and Sepsis

Sparstolonin B attenuates spinal cord injury‑induced inflammation in rats by modulating TLR4‑trafficking

Between Innovation and Standardization, Is There Still a Room for Scientific Reports? The Rise of a Formatting Tradition in Periodontal Research

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