Xijiao Dihuang decoction improves prognosis of sepsis via inhibition of aerobic glycolysis

Lü, Jun; Zhang, Luyao; Lu, Chuanyong; He, Sihao; Zhang, Yan; Yan, Jing; Zhou, Jiang

doi:10.1016/j.biopha.2020.110501

Cited by 16 publications

(15 citation statements)

References 21 publications

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“…Recent studies reported that XJDHT alleviates sepsis by reducing the release of proinflammatory cytokines. XJDHT can improve sepsis by suppressing aerobic glycolysis through downregulation of the TLR4/HIF-1α/PKM2 signalling pathway ( 194 ). Therefore, the treatment effect of XJDHT on sepsis indicates that cytokine release can be inhibited by modulating PKM2.…”

Section: Pkm2: a Potential Therapeutic Target Of Oxidative Stress And Inflammatory Damagementioning

confidence: 99%

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Liu

Chen

et al. 2021

Front. Immunol.

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The cytokine storm is a marker of severity of various diseases and increased mortality. The altered metabolic profile and energy generation of immune cells affects their activation, exacerbating the cytokine storm. Currently, the emerging field of immunometabolism has highlighted the importance of specific metabolic pathways in immune regulation. The glycolytic enzyme pyruvate kinase M2 (PKM2) is a key regulator of immunometabolism and bridges metabolic and inflammatory dysfunction. This enzyme changes its conformation thus walks in different fields including metabolism and inflammation and associates with various transcription factors. This review summarizes the vital role of PKM2 in mediating immunometabolic reprogramming and its role in inducing cytokine storm, with a focus on providing references for further understanding of its pathological functions and for proposing new targets for the treatment of related diseases.

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Section: Pkm2: a Potential Therapeutic Target Of Oxidative Stress And Inflammatory Damagementioning

confidence: 99%

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Liu

Chen

et al. 2021

Front. Immunol.

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“…Adult SD rats (weight 180-220 g, about 6-8 weeks old) were purchased from the experimental animal center of Zhejiang Academy of Medical Sciences (Zhejiang, China). Sepsis was induced by cecum ligation and puncture (CLP) as reported in previous studies [16,17]. The rats were anesthetized by intraperitoneal injection of 10% chloral hydrate at a dose of 0.3 ml/100 g. An incision of 2.5 cm from middle abdomen was performed under sterile conditions.…”

Section: Sepsis Model and Groupsmentioning

confidence: 99%

Interleukin-9 promotes intestinal barrier injury of sepsis: a translational research

et al. 2021

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Background Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Intestinal mucosal barrier injury is one of the important manifestations of sepsis. Interleukin-9 (IL-9) and IL-9-producing CD4(+) T cells were emerging pro-inflammatory mediators with development of intestinal injury. However, it is unclear whether IL-9 is related to the intestinal barrier injury of sepsis. Methods To investigate the roles of IL-9-producing CD4(+) T cells and IL-9 in the process of barrier injury in sepsis, serum IL-9-producing CD4(+) T cell percentages, IL-9, and D-lactate levels were measured in septic patients and controls. The markers of barrier function in serum and intestinal tissue were also collected in septic rats. Moreover, the barrier injury degree and survival rate of septic rats were also investigated after increasing or interfering with IL-9 expression. Results The serum IL-9-producing CD4(+) T cell percentages, IL-9, and D-lactate levels were significantly higher in septic patients or rats than those in controls. IL-9-producing CD4(+) T cells and IL-9 levels were positively correlated with D-lactate levels and had a high predictive value of 28-day mortality in septic patients. The non-survivors had significantly higher serum T cell percentages, IL-9, and D-lactate levels compared with survivors. In septic rats, IL-9 increased the expression levels of D-lactate, whereas that decreased the expression levels of zonula occludens 1. Moreover, the barrier injury was aggravated or alleviated by increasing or interfering with IL-9 expression, respectively. Survival rate analysis also showed that IL-9 decreased the 14-day survival rate of septic rats. Conclusion IL-9 is closely related to intestinal mucosal barrier injury and mortality in sepsis. IL-9 blockade has the potential to improve the barrier injury in sepsis. Trial registration The study was registered at ClinicalTrials.gov (ID: NCT03791866, Date: December 2018).

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“…Hypoxia-inducing factor 1 (HIF-1) signaling pathway is the channel that monocytes undergo reprogramming to generate immunosuppression in the late stage of sepsis [ 16 ]. It has been proved that downregulating the activated HIF-1α, the HDAC4 client transcription factor, could improve the prognosis of sepsis [ 17 ] and relieve myocardial injury during sepsis [ 18 ]. Enlightened by those studies, we would wonder that whether miR-124-3p could interact with SP1, thereby affecting HDAC4/HIF-1α axis to attenuate myocardial injury in sepsis.…”

Section: Introductionmentioning

confidence: 99%

microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis

Huang

Wen-fang

et al. 2022

Cell Death Discov.

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Sepsis-induced cardiac dysfunction can lead to death in sepsis. In this case, we targeted to explore in detail the relative mechanism of microRNA (miR)-124-3p in sepsis-induced myocardial injury via the specific protein 1/histone deacetylase 4/hypoxia-inducing factor 1α (SP1/HDAC4/HIF-1α) axis. Septic rats were modeled by cecal ligation puncture while in vitro septic cardiomyocyte H9C2 were induced by lipopolysaccharide (LPS). miR-124-3p/SP1/HDAC4/HIF-1α expression levels in myocardial tissues of septic rats and LPS-treated H9C2 cells were measured. miR-124-3p overexpression and SP1 silencing assays were implemented on LPS-treated H9C2 cells to explore theirs actions in inflammation, oxidative stress and cell apoptosis. The interactions of miR-124-3p, SP1, and HDAC4 were testified. miR-124-3p was lowly expressed while SP1, HDAC4, and HIF-1α were highly expressed in sepsis. Upregulation of miR-124-3p ameliorated inflammation, oxidative stress, and apoptosis of LPS-treated H9C2 cells. Silencing SP1 improved LPS-induced damage to cardiomyocytes. miR-124-3p targeted SP1 and HDAC4 interacted with SP1. SP1 overexpression antagonized miR-124-3p upregulation-induced improvements in LPS-induced cardiomyocyte damage. This study illustrates that miR-124-3p improves myocardial injury in septic rats through targeted regulation of SP1 to mediate HDAC4/HIF-1α.

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Xijiao Dihuang decoction improves prognosis of sepsis via inhibition of aerobic glycolysis

Cited by 16 publications

References 21 publications

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Interleukin-9 promotes intestinal barrier injury of sepsis: a translational research

microRNA-124-3p attenuates myocardial injury in sepsis via modulating SP1/HDAC4/HIF-1α axis

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