Dissection of the role of paeoniflorin in the traditional Chinese medicinal formula Si-Ni-San against contact dermatitis in mice

Sun, Yang; Dong, Yi; Jiang, Huijuan; Cai, Tiantian; Chen, Liang; Zhou, Xiang; Chen, Ting; Xu, Qiang

doi:10.1016/j.lfs.2008.12.023

Cited by 38 publications

(25 citation statements)

References 30 publications

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“…In the present study, LPS challenge markedly elevated the formation of NO and iNOS expression in mouse lung tissues. PF markedly suppressed the expressions of iNOS mRNA in lung tissues and decreased the levels of NO in BALF, which was consistent with previous findings that PF could decrease iNOS expression in LPS-stimulated human dermal microvascular endothelial cells and in ear tissues of contact dermatitis mice [37,38]. Taken together, the protection afforded by PF against LPS-induced ALI in mice is related to inhibition of proinflammatory cytokine production in lung tissues.…”

Section: Discussionsupporting

confidence: 91%

Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability

et al. 2011

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Section: Discussionsupporting

confidence: 91%

Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability

et al. 2011

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“…Traditional Chinese medicine that has been practiced for thousands of years in clinic often provides a vast source of pharmaceutical material for the development of effective drugs [Zhang and Tang, 2006;White, 2008]. The substantial obstacle, however, is that the detailed mechanisms of action of many of these natural active ingredients are largely unknown [Ren et al, 2008;Sun et al, 2009]. So finding effective anti-cancer natural compounds will not only facilitate our understanding of regulation for the network of cancer, but also provide some useful small probes for investigating the interactions of critical signaling molecules involved in cancer.…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to polydatin-induced apoptosis in human nasopharyngeal carcinoma CNE cells

et al. 2011

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Previous studies revealed that polydatin, a natural small compound, possessed protective effect against ischemia/reperfusion injury and inflammation. However, the action and molecular mechanism of its potent anti-cancer activity remain poorly understood. In the present study, polydatin significantly killed several human tumor cell lines in a dose- and time-dependent manner. The compound also dose-dependently caused mitochondrial apoptosis in human nasopharyngeal carcinoma CNE cells. In addition, polydatin triggered endoplasmic reticulum (ER) stress and down-regulated the phosphorylation of Akt in CNE cells, while knock-down of CCAAT/enhancer-binding protein homologous protein (CHOP) dramatically abrogated the inactivation of Akt and reversed the pro-apoptotic effect of polydatin. Furthermore, polydatin provoked the generation of reactive oxygen species in CNE cells, while the antioxidant N-acetyl cysteine almost completely blocked the activation of ER stress and apoptosis, suggesting polydatin-induced reactive oxygen species is an early event that triggers ER stress mitochondrial apoptotic pathways in CNE cells. Taken together, these findings strongly suggest that polydatin might be a promising anti-tumor drug and our data provide the molecular theoretical basis for clinical application of polydatin.

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“…Knowing that inflammation is the main contributing factor of inflammatory pain, we observed that analgesic effect of PF and explored its inhibitory mechanism. It was found in previous studies that PF could inhibit the inflammatory response of dendritic cells by blocking the signal pathway of toll-like receptor 4/5 (TLR4/5) [37], and PF inhibited the synthesis of TNF-α, NO, prostaglandin E2 (PE2) and other proinflammatory factors in the mononuclear macrophage system to relieve inflammation [38]. PF also had an inhibitory effect on inflammation in the CNS.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

Paeoniflorin Attenuates Inflammatory Pain by Inhibiting Microglial Activation and Akt-NF-κB Signaling in the Central Nervous System

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Paeoniflorin (PF) is known to have anti-inflammatory and paregoric effects, but the mechanism underlying its analgesic effect remains unclear. The aim of this study was to clarify the effect of PF on Freund’s complete adjuvant (CFA)-induced inflammatory pain and explore the underlying molecular mechanism. Methods: An inflammatory pain model was established by intraplantar injection of CFA in C57BL/6J mice. After intrathecal injection of PF daily for 8 consecutive days, thermal and mechanical withdrawal thresholds, the levels of inflammatory factors TNF-α, IL-1β and IL-6, microglial activity, and the expression of Akt-NF-κB signaling pathway in the spinal cord tissue were detected by animal ethological test, cell culture, enzyme-linked immunosorbent assay, immunofluorescence histochemistry, and western blot. Results: PF inhibited the spinal microglial activation in the CFA-induced pain model. The production of proinflammatory cytokines was decreased in the central nervous system after PF treatment both in vivo and in vitro. PF further displayed a remarkable effect on inhibiting the activation of Akt-NF-κB signaling pathway in vivo and in vitro. Conclusion: These results suggest that PF is a potential therapeutic agent for inflammatory pain and merits further investigation.

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Dissection of the role of paeoniflorin in the traditional Chinese medicinal formula Si-Ni-San against contact dermatitis in mice

Cited by 38 publications

References 30 publications

Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability

Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability

Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to polydatin-induced apoptosis in human nasopharyngeal carcinoma CNE cells

Paeoniflorin Attenuates Inflammatory Pain by Inhibiting Microglial Activation and Akt-NF-κB Signaling in the Central Nervous System

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