Corilagin protects the acute lung injury by ameliorating the apoptosis pathway

Guo, Shanshan; Fu, Yun; Xiong, Shenming; Lv, Jiudi

doi:10.1016/j.biopha.2017.09.034

Cited by 20 publications

(17 citation statements)

References 18 publications

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“…MPO levels in the corilagin-treated group were significantly reduced compared with those in the Con A-treated group ( Figure 2C ). These results are consistent with those of other studies on the antioxidant effects of corilagin on other mouse models, such as the acetaminophen-induced hepatotoxicity model and ischemia/reperfusion-induced acute lung injury model ( 28 , 29 , 36 ). Previous studies have shown that necrotic hepatocyte death induced by Con A is accompanied by massive apoptosis ( 35 , 37 ).…”

Section: Resultssupporting

confidence: 92%

Corilagin Ameliorates Con A-Induced Hepatic Injury by Restricting M1 Macrophage Polarization

et al. 2022

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Immune-mediated hepatic injury plays a key role in the initiation and pathogenesis of diverse liver diseases. However, treatment choice for immune-mediated hepatic injury remains limited. Corilagin, a natural ellagitannin extracted from various traditional Chinese medicines, has been demonstrated to exhibit multiple pharmacological activities, such as anti-inflammatory, anti-tumor, and hepatoprotective properties. The present study aimed to investigate the effects of corilagin on immune-mediated hepatic injury using a murine model of concanavalin A (Con A)-induced hepatitis, which is well-characterized to study acute immune-mediated hepatitis. Herein, mice were administered corilagin (25 mg/kg) intraperitoneally twice at 12 h intervals, and 1 h later, the mice were challenged with Con A (20 mg/kg body weight); serum and liver samples were collected after 12 h. The results showed that corilagin significantly increased the survival of mice and reduced serum alanine transaminase (ALT) and aspartate aminotransferase (AST) levels. In addition, corilagin markedly improved histopathological damage, hepatocyte apoptosis, and oxidative stress in the liver. The activation of M1 macrophages in the hepatic mononuclear cells was also significantly reduced compared with that in the control group. The expression of M1 macrophage-associated proinflammatory cytokines and genes, including interleukin (IL)-6, IL-12, and inducible nitric oxide synthase (iNOS), was also decreased after corilagin treatment. Finally, the results demonstrated that corilagin regulated macrophage polarization by modulating the mitogen-activated protein kinases (MAPK), nuclear factor (NF)-κB, and interferon regulatory factor (IRF) signaling pathways. Thus, the findings indicate that corilagin protects mice from Con A-induced immune-mediated hepatic injury by limiting M1 macrophage activation via the MAPK, NF-κB, and IRF signaling pathways, suggesting corilagin as a possible treatment choice for immune-mediated hepatic injury.

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Section: Resultssupporting

confidence: 92%

Corilagin Ameliorates Con A-Induced Hepatic Injury by Restricting M1 Macrophage Polarization

et al. 2022

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“…Corilagin 109 , a polyphenol of the tannin family, is isolated from Terminalia chebula Retz. This compound at 20 mg/kg obviously improved pulmonary function, inhibited inflammatory cytokines expression (TNF-α, COX-2, IL-6 and IL-1β) and suppressed lung cell apoptosis in I/R-induced ALI through blocking the JNK/MAPK pathway [ 328 ]. Additionally, corilagin attenuated bleomycin-induced lung injury and lung fibrosis through down-regulating the NF-κB and TGF-β1 signaling pathways [ 329 ].…”

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Zhou

et al. 2021

Pharmacological Research

250

121

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“…In addition, we observed an interesting phenomenon of no significant difference in the levels of IL-6, IL-10, or TNF-α in BALF between subgroups within the same group, and the trend in the level of these cytokines in serum was consistent with that in BALF. We considered that hypoxia and ischemia-reperfusion increased vascular permeability and the oxygen radical in the donor lung tissue, which enhanced the migration of inflammatory cells and the release of cytokines [3,20]. The inflammatory signal was also constantly amplified after the responding cells were influenced by various inflammatory factors in blood circulation, with the result that elevated plasma cytokines act on bilateral lung tissue.…”

Section: Discussionmentioning

confidence: 99%

Early Protection by Resveratrol in Rat Lung Transplantation

Wang

et al. 2019

Med Sci Monit

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BackgroundResveratrol is a multifunctional bioactive substance that has effects in anti-inflammation and prevention of ischemia-reperfusion injury. This study compared the inflammation and expression of related proteins during the early stages after transplantation to explore the effects and mechanisms of resveratrol on transplanted lung.Material/MethodsSprague-Dawley rats were randomized to receive pretreatment of resveratrol suspension (60 mg/kg; RES group), dexamethasone (1 mg/kg; DEM group), or normal saline solution (2 mL/kg; control group) 1 h before lung transplantation. The cytokine concentration in the serum and bronchoalveolar lavage fluid (BALF) of the recipients was determined 24 h after transplantation. Histopathologic evaluation, including lung injury score, and the expression of necroptosis-associated proteins was assessed.ResultsHistopathologic evaluation showed pneumocyte damage and endothelialitis associated with hemorrhage in the alveoli in the control group, the severity of which was greater than that in the other 2 groups. The levels of interleukin-6 and tumor necrosis factor-α in the serum and BALF of the RES and DEM groups were lower than those in the control group. The expression of necroptosis-associated proteins in the RES group was lower than that in the control group, and was inversely proportional to lung injury.ConclusionsPretreatment with resveratrol protected rat lung in the early stages after transplantation. We determined a relationship between necroptosis-associated proteins and transplanted lung injury, which suggests that the mechanism of lung transplantation-associated ischemia-reperfusion injury may be related to necroptosis.

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Corilagin protects the acute lung injury by ameliorating the apoptosis pathway

Cited by 20 publications

References 18 publications

Corilagin Ameliorates Con A-Induced Hepatic Injury by Restricting M1 Macrophage Polarization

Corilagin Ameliorates Con A-Induced Hepatic Injury by Restricting M1 Macrophage Polarization

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Early Protection by Resveratrol in Rat Lung Transplantation

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