Emodin alleviates lung injury in rats with sepsis

Yin, Jiang-Tao; Wan, Bing; Liu, Dadong; Wan, Shengxia; Fu, Haiyan; Wan, Yin; Zhang, Hao; Chen, Yikun

doi:10.1016/j.jss.2015.12.049

Cited by 26 publications

(23 citation statements)

References 20 publications

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“…And these typical pathological changes were remarkably improved by E/S treatment or Emodin. Although Emodin showed protective effects on lung injury, which was consistent with the results of Yin's report (Yin et al, 2016), E/S showed a much stronger inhibition than Emodin, indicating that E/S can strength the effects of Emodin or nanosilver and weak the toxicity of nanosilver.…”

Section: Discussionsupporting

confidence: 90%

Emodin Combined with Nanosilver Inhibited Sepsis by Anti-inflammatory Protection

Zhou

et al. 2017

Front. Pharmacol.

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Background: Emodin is the main active component of rhubarb, which has demonstrated many beneficial effects against inflammation. Nanosilver is an effective antimicrobial agent. The present study was designed to observe the effects of Emodin combined with silver nanoparticles (E/S) on sepsis protection and related mechanism.Methods: E/S was prepared by loading different concentrations of Emodin on nanosilver and cytotoxicity of E/S were determined by suphorhodamine B assays. Anti-microbial activities of E/S were assayed by direct interaction with various common pathogens and anti-adhesive activites of E/S on leukocytes with endothelial cells were assayed by biochemical analysis. Next, inflammatory cell enumeration, inflammatory mediators in bronchoalveolar lavage fluid (BALF) and endothelial cell function were analyzed on a clinically relevant model of sepsis induced by cecal ligation and puncture (CLP) after E/S administration. The effects of E/S on NF-κB and p38 were also examined by western blot.Results: E/S exhibited little cytotoxicity action on endothelial cells and significant inhibitory activities against all tested common microorganisms and adherence between leukocyte and endothelial cells. E/S induced anti-sepsis protection mainly mediated by inhibition of inflammatory cells infiltration, down-regulation of TNF-alpha, IL-8 and lactic dehydrogenase (LDH), and inhibition of NF-κB and p38 pathways in mice 24 h post-CLP.Conclusion: Our data suggest that E/S has strong anti-sepsis effects, which was related with anti-inflammatory protection and thereby promote survival following sepsis challenge.

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Section: Discussionsupporting

confidence: 90%

Emodin Combined with Nanosilver Inhibited Sepsis by Anti-inflammatory Protection

Zhou

et al. 2017

Front. Pharmacol.

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“…Emodin can also promote cell apoptosis and reduce necrosis occurring in the pancreatic acinar cell or inflammatory cells, for example, emodin inhibits SIRS in SAP rats via inducing neutrophil apoptosis via the calcium-mediated caspase-12 signaling pathway (Ni et al, 2014b; Yin et al, 2016). In addition, the protective effects of emodin on ER stress responses are mediated by significantly attenuating calcium overload and decreasing the expression of ER chaperone immunoglobulin-binding protein (Bip), PERK, ATF6, IRE1α, TRAF2 and ASK1, as well as inhibiting the phosphorylation of MAPKs (Wu et al, 2013, 2014).…”

Section: Pleiotropic Natural Productsmentioning

confidence: 99%

Chinese Herbal Medicines Attenuate Acute Pancreatitis: Pharmacological Activities and Mechanisms

Xiang

Zhang

et al. 2017

Front. Pharmacol.

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Acute pancreatitis (AP) is a commonly occurring gastrointestinal disorder. An increase in the annual incidence of AP has been observed, and it causes acute hospitalization and high mortality. The diagnosis and treatment guidelines for AP recommend conservative medical treatments focused on reducing pancreatic secretion and secondary injury, as a primary therapeutic approach. Unfortunately, the existing treatment options have limited impact on the incidence and severity of AP due to the complex and multifaceted pathological process of this disease. In recent decades, Chinese herbal medicines (CHMs) have been used as efficient therapeutic agents to attenuate AP in Asian countries. Despite early cell culture, animal models, and clinical trials, CHMs are capable of interacting with numerous molecular targets participating in the pathogenesis of AP; however, comprehensive, up-to-date communication in this field is not yet available. This review focuses on the pharmacological activities of CHMs against AP in vitro and in vivo and the underlying mechanisms. A computational prediction of few selected and promising plant-derived molecules (emodin, baicalin, resveratrol, curcumin, ligustrazine, and honokiol) to target numerous proteins or networks involved in AP was initially established based on a network pharmacology simulation. Moreover, we also summarized some potential toxic natural products for pancreas in order to more safe and reasonable medication. These breakthrough findings may have important implications for innovative drug research and the future development of treatments for AP.

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“…Inactivation of MAPK signaling by emodin has also been documented in several other biological conditions (19,20). For instance, in a rat model of sepsis, emodin attenuated lung injury through inhibition of p38 MAPK (20). The regulation of ROS production and MAPK activation may represent an important mechanism for the protection against H/R-induced cellular injury induced by emodin.…”

Section: Discussionmentioning

confidence: 93%

Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation

Chen

Huang

Xiang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to determine the effects of emodin, a natural compound with antioxidant properties, on oxidative stress and apoptosis induced by hypoxia/reoxygenation (H/R) in HK-2 human renal tubular cells. In HK-2 cells subjected to H/R, it was observed that pre-treatment with emodin lead to an increase in cellular viability and a reduction in the rate of apoptosis and the B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 ratio. H/R alone caused a significant increase in the levels of reactive oxygen species and malondialdehyde (P<0.05) and a significant decrease in the activities of superoxide dismutase, catalase and glutathione peroxidase (P<0.05), relative to normoxic cells. In turn, parameters of oxidative stress were improved by emodin pre-treatment. In addition, emodin pre-treatment significantly inhibited the phosphorylation of extracellular signal-regulated protein kinase and c-Jun N-terminal kinase mitogen-activated protein kinases (MAPKs) induced by H/R (P<0.05). These data suggest that emodin may prevent H/R-induced apoptosis in human renal tubular cells through the regulation of cellular oxidative stress, MAPK activation and restoration of the Bax/Bcl-2 ratio.

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Emodin alleviates lung injury in rats with sepsis

Cited by 26 publications

References 20 publications

Emodin Combined with Nanosilver Inhibited Sepsis by Anti-inflammatory Protection

Emodin Combined with Nanosilver Inhibited Sepsis by Anti-inflammatory Protection

Chinese Herbal Medicines Attenuate Acute Pancreatitis: Pharmacological Activities and Mechanisms

Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation

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