Emodin Attenuates Severe Acute Pancreatitis via Antioxidant and Anti-inflammatory Activity

Xia, Shilin; Ni, Yujia; Zhou, Qi; Liu, Han; Xiang, Hong; Sui, Hua; Shang, Dong

doi:10.1007/s10753-019-01077-z

Cited by 75 publications

(55 citation statements)

References 39 publications

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“…The improvement of antioxidant and anti-inflammatory properties is the potential approaches for preventing SAP progression [23,24]. In the present work, picroside II protected rats against SAP development by increasing antioxidant and anti-inflammatory capacities (Figures 3 and 4).…”

Section: Discussionsupporting

confidence: 55%

Picroside II Improves Severe Acute Pancreatitis-Induced Intestinal Barrier Injury by Inactivating Oxidative and Inflammatory TLR4-Dependent PI3K/AKT/NF-κB Signaling and Improving Gut Microbiota

Piao¹,

Liu

Sui

et al. 2020

Oxidative Medicine and Cellular Longevity

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Background. Picroside II exerts anti-inflammatory and antidiarrheal effects for treating the diseases associated with oxidative injury. However, its function on pancreatitis-induced intestinal barrier injury remains unclear. Hypothesis/Purpose. We hypothesized that picroside II will have protective effects against pancreatitis-induced intestinal barrier injury by affecting oxidative and inflammatory signaling (Toll-like receptor 4- (TLR4-) dependent phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), and nuclear factor kappa B (NF-κB)). Study Design and Methods. A Sprague-Dawley (SD) rat model with severe acute pancreatitis (SAP) was induced via the injection of sodium taurocholate (4% wt/vol; 1 mL/kg). All rats were divided into 3 groups: sham (CG), SAP-induced intestinal barrier injury (MG), and picroside II (PG) groups. Intestinal barrier injury was assessed by scanning electron microscopy (SEM), hematoxylin and eosin staining, and pathological scores. We measured the levels of pancreatitis biomarkers (amylase and lipase), oxidative and inflammatory signaling (TLR4-dependent PI3K/AKT/NF-κB), oxidative stress marker (superoxidase dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx), and malondialdehyde), and inflammatory markers (tumor necrosis factor α (TNFα), interleukin- (IL-) 1, IL-6, and IL-10) in serum and/or gut tissues. Gut microbiota composition in feces was measured by using 16S rRNA sequencing. Results. SEM showed that intestinal barrier injury was caused with the loss of intestinal villi and mitochondria destruction, and pathological scores were increased in the MG group. The levels of amylase, lipase, malondialdehyde, TNFα, IL-1, IL-6, TLR4, PI3K, AKT, and NF-κB were increased, and the levels of SOD, GPx, CAT, and IL-10 was reduced in the MG group when compared with CG group (P<0.05). Picroside II treatment inhibited the symptoms in the MG group and showed antioxidant and anti-inflammatory activities. The serum levels of picroside II had strong correlation with the levels of inflammatory and oxidative stress biomarkers (P<0.05). Picroside II treatment increased the proportion of Lactobacillus and Prevotella and decreased the proportion of Helicobacter and Escherichia_Shigella in the model. Conclusions. Picroside II improved the SAP-induced intestinal barrier injury in the rat model by inactivating oxidant and inflammatory signaling and improving gut microbiota.

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Section: Discussionsupporting

confidence: 55%

Picroside II Improves Severe Acute Pancreatitis-Induced Intestinal Barrier Injury by Inactivating Oxidative and Inflammatory TLR4-Dependent PI3K/AKT/NF-κB Signaling and Improving Gut Microbiota

Piao¹,

Liu

Sui

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Thus, the protective effect of emodin against CLP-induced intestinal barrier injury can be partially explained by the increased expression of TJ proteins. In recent years, numerous scientific reports described that emodin has an anti-inflammatory effect and can reduce the expression of the inflammatory factor TNF-α (55)(56)(57). Compared with expression in the corresponding CLP group, the protein expression levels of claudin-3 in the CLP + emodin group showed a continuous and uniform distribution, with a smoother edge and an enhanced positive signal.…”

Section: Discussionmentioning

confidence: 91%

Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Guo

Zhang

et al. 2020

Exp Ther Med

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Αbstract. The present study investigated the protective effects of emodin on intestinal epithelial tight junction (TJ) barrier integrity in cecal ligation and puncture (CLP)-induced septic rats and its possible mechanisms of action. Healthy male Sprague-Dawley rats were randomly divided into three groups (n=20 per group): Sham group, CLP group and CLP + emodin group. Animals were sacrificed at 12 and 24 h after the model was established. Abdominal aortic blood and specimens of the ileum were harvested for analysis. The histopathological changes in intestinal mucosa and the ultrastructures of intestinal epithelial cells were investigated using light microscopy and transmission electron microscopy. The integrity of the intestinal barrier was assessed by examining plasma diamine oxidase (DAO) levels and the ratio of urine lactulose to mannitol (L/M). The levels of the intestinal TJ proteins claudin-3, zonula occludens (ZO)-1 and occludin were detected using immunohistochemistry, western blotting and reverse transcription-quantitative PCR. The results showed that the pathological damage to intestinal mucosa and the intestinal tissue injury score in the CLP + emodin group were significantly reduced compared to those of the CLP group, and the differences were more obvious at 24 h compared with 12 h. DAO activity and the L/M ratio in the emodin pre-treatment group decreased significantly at 24 h compared with the CLP groups. The protein and mRNA levels of the TJ proteins claudin-3, ZO-1 and occludin in the emodin pre-treatment groups at 12 and 24 h were increased, while occludin mRNA level was found to be decreased compared with the CLP groups. The present study suggested that emodin may significantly reduce the damage to the intestinal epithelial barrier in sepsis, inhibit intestinal barrier permeability and protect intestinal barrier integrity. Emodin may protect intestinal barrier integrity by elevating expression levels of the TJ proteins claudin-3, ZO-1 and occludin in CLP rats.

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“…Neutrophils are over-activated during ALI, which releases neutrophil respiratory burst and ROS to damage the surrounding tissues [30] . Our experimental results supported this conclusion.…”

Section: Discussionmentioning

confidence: 99%

“…During an inflammatory injury, neutrophils gather at the injury site to exert phagocytosis, an important aspect of neutrophils to kill pathogenic microorganisms [30] . Our study found that Emo promotes phagocytosis of neutrophils: the phagocytosis of S.aureus and E.coli by neutrophils increases with time, reaching a peak at 60 min.…”

Section: Discussionmentioning

confidence: 99%

Emodin alleviates LPS-induced inflammatory response in lung injury mice by affecting the function of neutrophils

Mei

Tao

Zhang

et al. 2020

Preprint

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Background: This study aims to investigate the role of Emodin(Emo) on the pulmonary inflammatory response and the neutrophil function in a murine model of lipopolysaccharide (LPS)-induced ALI. The mouse model of lipopolysaccharide (LPS)-induced ALI was produced by acute lung injury of injecting 20 mg/kg LPS via the caudal vein.The right lower lung lobes were harvested, fixed,embedded and stained with hematoxylin and eosin (H&E) for light microscopy analysis to evaluate lung injury. TNF-αand IL-1 ELISA kits were used to detect the levels of TNF-α and IL-1 in the right lung homogenate of rats. The primary rat neutrophils were separated and treated with LPS to mimic a ALI cellular model. The expression of Respiratory burst and Neutrophil NETs Production was examined using spectrophotometer.The Elastase release was detected using Elastase Activity Assay kit.The ROS Production was measured by Luminometer.the phagocytosis of Neutrophils and the rate of apoptotic Neutrophils were measured by flow cytometry. Results: This study demonstrates that Emo alleviates lung injury and reduces the release of inflammatory cytokines. Moreover, Emo also downregulated neutrophil respiratory burst and the production of ROS in the LPS-stimulated neutrophils, thus reducing the damage of neutrophils to the surrounding tissues. Emo can also up-regulate the ability of neutrophils to phagocytize bacteria and generate NETs, thereby enhancing the bactericidal ability of neutrophils. In addition, Emo can promote the apoptosis of neutrophils and accelerate the resolution of inflammation. Conclusion: Emo has a protection effect on LPS-induced acute lung injury mice. It can alleviate lung injury and reduces the release of inflammatory cytokines, perhaps by affecting the various function of neutrophils in a dose-dependent manner.

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Emodin Attenuates Severe Acute Pancreatitis via Antioxidant and Anti-inflammatory Activity

Cited by 75 publications

References 39 publications

Picroside II Improves Severe Acute Pancreatitis-Induced Intestinal Barrier Injury by Inactivating Oxidative and Inflammatory TLR4-Dependent PI3K/AKT/NF-κB Signaling and Improving Gut Microbiota

Picroside II Improves Severe Acute Pancreatitis-Induced Intestinal Barrier Injury by Inactivating Oxidative and Inflammatory TLR4-Dependent PI3K/AKT/NF-κB Signaling and Improving Gut Microbiota

Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Emodin alleviates LPS-induced inflammatory response in lung injury mice by affecting the function of neutrophils

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