Emodin alleviates jejunum injury in rats with sepsis by inhibiting inflammation response

Chen, Yi‐Kun; Xu, Yingkun; Zhang, Hao; Yin, Jie; Fan, Xiaoxuan; Liu, Dadong; Fu, Haiyan; Wan, Bing

doi:10.1016/j.biopha.2016.10.031

Cited by 45 publications

(37 citation statements)

References 21 publications

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“…Emodin has been shown to reduce septic jejunal damage by inhibiting apoptosis of intestinal epithelial cells through anti-inflammatory effects (35). In the present study, light microscopy and electron microscopy were used to observe the pathological changes in the intestinal mucosal epithelium.…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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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“…Previous research has indicated that rhubarb has potent anti-inflammatory activity and its active ingredient, rhubarb acid, has been reported to reduce liver and kidney damage (8). Previous studies by our group have indicated that a compound contained in Chinese rhubarb, emodin, inhibits the body's inflammatory response and reduce organ damage from acute pancreatitis or sepsis (9,10). In the present clinical study, rhubarb was administrated as a supplementary treatment for patients with heat stroke.…”

Section: Introductionmentioning

confidence: 81%

“…Emodin, one of the active components of rhubarb, activates the Janus kinase (JAK)1/signal transducer and activator of transcription (STAT)3 signaling pathway to protect the jejunum in sepsis patients (10). Emodin was also reported to inhibit oxidative stress and inflammatory response to lung injury via the p38 mitogen-activated protein kinase pathway during sepsis and significantly alleviate sodium taurocholate-induced pancreatic acinar cell injury by decreasing the release of inflammatory factors (tumor necrosis factor-α, IL-1β and IL-6) (23,24).…”

Section: Discussionmentioning

confidence: 99%

Adjuvant rhubarb alleviates organs dysfunction and inhibits inflammation in heat stroke

Wan

Sun

et al. 2018

Exp Ther Med

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The aim of the present study was to investigate the effects of adjuvant rhubarb on the recovery of patients with heat stroke. A total of 85 patients with heat stroke were randomly assigned to two treatment groups: One group receiving conventional treatment for heat stroke (conventional group) and one group receiving rhubarb supplement in addition to conventional treatment (rhubarb group). Liver and kidney function parameters, Acute Physiology and Chronic Health Evaluation (APACHE) II scores, plasma interleukin-6 (IL-6), procalcitonin (PCT), C-reactive protein (CRP) levels and venous white blood cell count (WBC) were analyzed. The length of stay in the intensive care units (ICUs) and hospital were recorded. Kaplan-Meier curves were drawn to determine the 30-day survival of the patients. The results indicated that rhubarb supplementation significantly reduced the WBC, as well as CRP, PCT and IL-6 levels at treatment days 3-5. Furthermore, rhubarb intake was observed to limit heat stroke-induced damage to liver and kidney function by decreasing the abnormally high levels of plasma aspartate aminotransferase, alanine aminotransferase and creatinine. Finally, patients in the rhubarb group had shorter ICU and hospital stays as well as a lower APACHE II score than those in the conventional group. However, no significant difference in the 30-day mortality rate was observed between the two groups. In conclusion, rhubarb intake provided a significant benefit for patients with heat stroke by inhibiting systemic inflammation and mitigating liver and kidney injury.

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“…The amount of active oxygen produced can be inferred from this data. The determination of neutrophil respiratory burst was slightly modified by reference [26] . ① Set blank control group C1, control group C2 and 5 test groups, and the appropriate amount of KRB was added in each group, 100 μl of cytochrome C (1.5 mg/ml) and 100 μl neutrophils (2×10 7 /ml) was then added; ②10μl SOD (5000 U/ml) was added, and the corresponding dose was added to the test group, equilibrated in a 5% CO 2 incubator at 37 °C for 10min; ③ 10 μl cytochalasin B (1mmol/L) was added to each group and after 3min, 10 μl fMLP (0.1mmol/L) was added for a total of 1 ml and each group was incubated in a 5% CO 2 incubator at 37°C for 30min; ④ Each group was removed and centrifuged at 2000r/min for 10 min;⑤ Supernatant was collected and the OD value was measured with a spectrophotometer.…”

Section: Respiratory Burst Detectionmentioning

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 alleviates jejunum injury in rats with sepsis by inhibiting inflammation response

Cited by 45 publications

References 21 publications

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

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

Adjuvant rhubarb alleviates organs dysfunction and inhibits inflammation in heat stroke

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

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