Protective effects of Lizhong decoction on ulcerative colitis in mice by suppressing inflammation and ameliorating gut barrier

Shen, Yi; Zou, Junfeng; Chen, Mengjun; Zhang, Zhimiao; Liu, Chen; Jiang, Shu; Qian, Dawei; Duan, Jin‐Ao

doi:10.1016/j.jep.2020.112919

Cited by 43 publications

(29 citation statements)

References 57 publications

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“…Previous studies have reported the therapeutic effects of several TCMs such as Lizhong Decoction, 371 Liujunzi Decoction, 372 and Huanglian Jiedu Decoction 373 on inflammatory diseases. Recently, TCM treatment has also been shown effective for COVID-19 and contributed substantially to control the pandemic in China.…”

Section: Interventions Targeting Multiple Cytokines and Pathwaysmentioning

confidence: 99%

The signal pathways and treatment of cytokine storm in COVID-19

Yang

Xie

et al. 2021

Sig Transduct Target Ther

443

413

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The Coronavirus Disease 2019 (COVID-19) pandemic has become a global crisis and is more devastating than any other previous infectious disease. It has affected a significant proportion of the global population both physically and mentally, and destroyed businesses and societies. Current evidence suggested that immunopathology may be responsible for COVID-19 pathogenesis, including lymphopenia, neutrophilia, dysregulation of monocytes and macrophages, reduced or delayed type I interferon (IFN-I) response, antibody-dependent enhancement, and especially, cytokine storm (CS). The CS is characterized by hyperproduction of an array of pro-inflammatory cytokines and is closely associated with poor prognosis. These excessively secreted pro-inflammatory cytokines initiate different inflammatory signaling pathways via their receptors on immune and tissue cells, resulting in complicated medical symptoms including fever, capillary leak syndrome, disseminated intravascular coagulation, acute respiratory distress syndrome, and multiorgan failure, ultimately leading to death in the most severe cases. Therefore, it is clinically important to understand the initiation and signaling pathways of CS to develop more effective treatment strategies for COVID-19. Herein, we discuss the latest developments in the immunopathological characteristics of COVID-19 and focus on CS including the current research status of the different cytokines involved. We also discuss the induction, function, downstream signaling, and existing and potential interventions for targeting these cytokines or related signal pathways. We believe that a comprehensive understanding of CS in COVID-19 will help to develop better strategies to effectively control immunopathology in this disease and other infectious and inflammatory diseases.

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Section: Interventions Targeting Multiple Cytokines and Pathwaysmentioning

confidence: 99%

The signal pathways and treatment of cytokine storm in COVID-19

Yang

Xie

et al. 2021

Sig Transduct Target Ther

443

413

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“…Myeloperoxidase (MPO), a glycoprotein promoting a series of peroxidative stress responses when neutrophils are stimulated, is a key marker reflecting the development of intestinal inflammation [ 26 ]. Diamine oxidase reflects intestinal mucosal injury and intestinal barrier [ 27 ].…”

Section: Resultsmentioning

confidence: 99%

Ficus pandurata Hance Inhibits Ulcerative Colitis and Colitis‐Associated Secondary Liver Damage of Mice by Enhancing Antioxidation Activity

Dai

Zhan

Peng

et al. 2021

Oxidative Medicine and Cellular Longevity

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Inflammatory bowel disease (IBD), a global disease threatening human health, is commonly accompanied by secondary liver damage (SLD) mediated by the gut-liver axis. Oxidative stress acts a critical role in the onset of IBD, during which excessive oxidation would destroy the tight junctions between intestinal cells, promote proinflammatory factors to penetrate, and thereby damage the intestinal mucosa. Ficus pandurata Hance (FPH) is widely used for daily health care in South China. Our previous study showed that FPH protected acute liver damage induced by alcohol. However, there is no study reporting FPH treating ulcerative colitis (UC). This study is designed to investigate whether FPH could inhibit UC and reveal its potential mechanism. The results showed that FPH significantly alleviated the UC disease symptoms including the body weight loss, disease activity index (DAI), stool consistency changing, rectal bleeding, and colon length loss of UC mice induced by dextran sulfate sodium (DSS) and reversed the influences of DSS on myeloperoxidase (MPO) and diamine oxidase activity (DAO). FPH suppressed UC via inhibiting the TLR4/MyD88/NF-κB pathway and strengthened the gut barrier of mice via increasing the expressions of ZO-1 and occludin and enhancing the colonic antioxidative stress property by increasing the levels of T-SOD and GSH-Px and the expressions of NRF2, HO-1, and NQO1 and reducing MDA level and Keap1, p22-phox, and NOX2 expressions. Furthermore, FPH significantly inhibited SLD related to colitis by reducing the abnormal levels of the liver index, ALT, AST, and cytokines including TNFα, LPS, LBP, sCD14, and IL-18 in the livers, as well as decreasing the protein expressions of NLRP3, TNFα, LBP, CD14, TLR4, MyD88, NF-κB, and p-NF-κB, suggesting that FPH alleviated UC-related SLD via suppressing inflammation mediated by inhibiting the TLR4/MyD88/NF-κB pathway. Our study firstly investigates the anticolitis pharmacological efficacy of FPH, suggesting that it can be enlarged to treat colitis and colitis-associated liver diseases in humans.

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“…For occludin, the expression level in both HP and LP groups showed no significant difference with that of the N group ( Figure 7 B). Claudin, occludin, and ZO-1 are the main components of tight junction, which is the most significant structure in the intestinal mucosal mechanical barrier [ 10 ]. The tight junction can effectively prevent enteric pathogens, antigens, and other substances from entering the intestinal mucosa, preventing the activation of immune cells and abnormal immune responses and maintaining stability of mucosal barrier function and intestinal permeability [ 36 ].…”

Section: Resultsmentioning

confidence: 99%

“…Numerous reports have testified to inflammatory reactions being a crucial factor causing UC [ 9 ]. The cytokines secreted by intestinal epithelial cells are important markers of the intestinal immune system and regulate their inflammatory responses [ 10 ]. Pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-1β can promote an inflammatory response, eventually causing colon tissue injury, while anti-inflammatory cytokines such as IL-4 and IL-10 can reduce inflammation [ 11 ].…”

Section: Introductionmentioning

confidence: 99%