Puerarin inhibits hyperglycemia-induced inter-endothelial junction through suppressing endothelial Nlrp3 inflammasome activation via ROS-dependent oxidative pathway

Lian, Dawei; Yuan, Huiqi; Yin, Xiong-Zhang; Wu, Yanjiao; He, Rong‐Rong; Huang, Yi; Chen, Yang

doi:10.1016/j.phymed.2018.10.013

Cited by 65 publications

(54 citation statements)

References 35 publications

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“…NLRP3 inflammasome-specific pharmacological inhibitors for the treatment of endothelial dysfunction NLRP3 inflammasome is involved in the progress of a variety of disorders, which promotes the discovery of NLRP3 inflammasome inhibitors. A large number of inhibitors have been demonstrated to improve endothelial dysfunction by inhibiting NLRP3 inflammasome signaling pathway, including endogenous and exogenous inhibitors, but with low specificity [107][108][109] . Here, we show the potential of specific NLRP3 inhibitors to ameliorate endothelial dysfunction (Table 3), which are briefly discussed below.…”

Section: Other Anti-inflammatory or Antioxidant Drugsmentioning

confidence: 99%

NLRP3 inflammasome in endothelial dysfunction

et al. 2020

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Inflammasomes are a class of cytosolic protein complexes. They act as cytosolic innate immune signal receptors to sense pathogens and initiate inflammatory responses under physiological and pathological conditions. The NLR-family pyrin domain-containing protein 3 (NLRP3) inflammasome is the most characteristic multimeric protein complex. Its activation triggers the cleavage of pro-interleukin (IL)-1β and pro-IL-18, which are mediated by caspase-1, and secretes mature forms of these mediators from cells to promote the further inflammatory process and oxidative stress. Simultaneously, cells undergo pro-inflammatory programmed cell death, termed pyroptosis. The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage. Vascular endothelium at the site of inflammation is actively involved in the regulation of inflammation progression with important implications for cardiovascular homeostasis as a dynamically adaptable interface. Endothelial dysfunction is a hallmark and predictor for cardiovascular ailments or adverse cardiovascular events, such as coronary artery disease, diabetes mellitus, hypertension, and hypercholesterolemia. The loss of proper endothelial function may lead to tissue swelling, chronic inflammation, and the formation of thrombi. As such, elimination of endothelial cell inflammation or activation is of clinical relevance. In this review, we provided a comprehensive perspective on the pivotal role of NLRP3 inflammasome activation in aggravating oxidative stress and endothelial dysfunction and the possible underlying mechanisms. Furthermore, we highlighted the contribution of noncoding RNAs to NLRP3 inflammasome activation-associated endothelial dysfunction, and outlined potential clinical drugs targeting NLRP3 inflammasome involved in endothelial dysfunction. Collectively, this summary provides recent developments and perspectives on how NLRP3 inflammasome interferes with endothelial dysfunction and the potential research value of NLRP3 inflammasome as a potential mediator of endothelial dysfunction.

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Section: Other Anti-inflammatory or Antioxidant Drugsmentioning

confidence: 99%

NLRP3 inflammasome in endothelial dysfunction

et al. 2020

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“…Puerarin may be an effective preventive compound against various nervous system diseases by regulating apoptosis and the inflammatory response (6). Puerarin inhibits the formation and activation of Nlrp3 inflammasome, which is induced by high glucose (7). In addition, puerarin exerts antioxidative effects and scavenges reactive oxygen species in cells.…”

mentioning

confidence: 99%

Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition

Zhou

Xue

Wang

et al. 2020

Braz J Med Biol Res

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Erratum for: "Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition" [Braz J Med Biol Res (2020) 53(4): e8882] Yuan Zhou 0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0The authors would like to correct the Corresponding authors' names and emails and the Acknowledgments section of the article "Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition". The Editors highlight that the information presented in the original version was provided by the authors at submission and revision. In addition, the authors had the opportunity to correct the information during proofreading, before approving for publication.Correspondence: Haozhen Ren: orenhaozhen1984@163.com4 | Jinglin Wangocw20120817@163.com4 *These authors contributed equally to this study.Braz J Med Biol Res | AbstractHepatocellular carcinoma (HCC) is one of the most common primary malignant tumors of the liver worldwide. Liver resection and transplantation are currently the only effective treatments; however, recurrence and metastasis rates are still high. Previous studies have shown that the epithelial-mesenchymal transition (EMT) is a key step in HCC invasion and metastasis. Inhibition of EMT has become a new therapeutic strategy for tumors. Recently, puerarin, a well-characterized component of traditional Chinese medicine, has been isolated from Pueraria radix and exerts positive effects on many diseases, particularly cancers. In this study, CCK-8, EdU immunofluorescence, colony formation, wound healing, and migration assays were used to detect the effects of puerarin on HCC cells. We further analyzed the relationship between puerarin and miR-21/PTEN/EMT markers in HCC cell lines. Our results showed that HCC cell proliferation, migration, invasion, tumor formation, and metastasis were reduced by puerarin in vitro and in vivo. Additionally, puerarin inhibited the EMT process of HCC by affecting the expression of Slug and Snail. Moreover, oncogenic miR-21 was inhibited by puerarin, coupled with an increase in the tumor suppressor gene PTEN. Increasing miR-21 expression or decreasing PTEN expression reversed the inhibition effects of puerarin in HCC. These data confirmed that puerarin affects HCC through the miR-21/PTEN/EMT regulatory axis. Overall, puerarin may represent a chemopreventive and/or chemotherapeutic agent for HCC treatment.

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“…NLRP3 inflammasome contributes to the increased release of high mobility group box1 (HMGB1), 19 one of the major damage‐associated molecular patterns (DAMPs). The protective mechanisms of other effective drugs have been shown to prevent endothelial dysfunction related to NLRP3 inflammasome, such as Asprin 20 and puerarin 21 . It has also been reported that AE possesses anti‐inflammatory effect.…”

Section: Introductionmentioning

confidence: 99%

“…The protective mechanisms of other effective drugs have been shown to prevent endothelial dysfunction related to NLRP3 inflammasome, such as Asprin 20 and puerarin. 21 It has also been reported that AE possesses anti-inflammatory effect.…”

mentioning

confidence: 97%

Aloe emodin relieves Ang II-induced endothelial junction dysfunction via promoting ubiquitination mediated NLRP3 inflammasome inactivation

Zhang

Song

Huang

et al. 2020

Journal of Leukocyte Biology

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Recent studies have revealed that aloe emodin (AE), a natural compound from the root and rhizome of Rheum palmatum L., exhibits significant pharmacologic activities. However, the pharmacologic relevance of the compound, particularly for cardiovascular disease, remains largely unknown. Here, we hypothesized that AE could improve endothelial junction dysfunction through inhibiting the activation of NOD-like receptor family pyrin domain containing-3 (NLRP3) inflammasome regulated by NLRP3 ubiquitination, and ultimately prevent cardiovascular disease. In vivo, we used confocal microscopy to study the expression of tight junction proteins zonula occludens-1/2 (ZO-1/2) and the formation of NLRP3 inflammasome in coronary arteries of hypertension. And the experimental serum was used to detect the activation of NLRP3 inflammasome by ELISA assay. We found that AE could restore the expression of the endothelial connective proteins ZO-1/2 and decrease the release of high mobility group box1 (HMGB1), and also inhibited the formation and activation of NLRP3 inflammasome. Similarly, in vitro, our findings demonstrated that AE could restore the expression of the tight junction proteins ZO-1/2 and decrease monolayer cell permeability that related to endothelial function after stimulation by angiotensin II (Ang II) in microvascular endothelial cells (MECs). We also demonstrated that AE could inhibit Ang II-induced NLRP3 inflammasome formation and activation, which were regulated by NLRP3 ubiquitination in MECs, as shown by fluorescence confocal microscopy and Western blot. Together with these changes, we revealed a new protection mechanism of AE that inhibited NLRP3 inflammasome activation and decreased the release of HMGB1 by promoting NLRP3 ubiquitination. Our findings implicated that AE exhibited immense potential and specific therapeutic value in hypertension-related cardiovascular disease in the early stage and the development of innovative drugs.

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Puerarin inhibits hyperglycemia-induced inter-endothelial junction through suppressing endothelial Nlrp3 inflammasome activation via ROS-dependent oxidative pathway

Cited by 65 publications

References 35 publications

NLRP3 inflammasome in endothelial dysfunction

NLRP3 inflammasome in endothelial dysfunction

Puerarin inhibits hepatocellular carcinoma invasion and metastasis through miR-21-mediated PTEN/AKT signaling to suppress the epithelial-mesenchymal transition

Aloe emodin relieves Ang II-induced endothelial junction dysfunction via promoting ubiquitination mediated NLRP3 inflammasome inactivation

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