Systemic inflammation and sepsis. Part II: Functional consequences of the storm

Dartiguelongue, Juan B

doi:10.5546/aap.2021.eng.e1

Cited by 3 publications

(1 citation statement)

References 89 publications

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“…Sepsis is a life-threatening complication of pneumonia, including pneumonia caused by coronavirus disease (Li et al 2021b). No organ is exempt from sepsis-induced dysfunction, such as heart (Dartiguelongue 2021; Poveda-Jaramillo 2021). Sepsis is a frequently lethal state, commonly associated with dysfunction of left ventricular (LV) (Cavefors et al 2021).…”

Section: Introductionmentioning

confidence: 99%

Midkine exacerbates inflammation, apoptosis and oxidative stress in heart of septic mice

Wei

Liu

et al. 2023

Preprint

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Aim: Midkine inhibition ameliorates sepsis induced lung injury. This research was to explore the influences of midkine on the sepsis-associated heart damage and the mechanisms. Methods: Sepsis models were established via lipopolysaccharide (LPS) induction in mice in vivo, and in HL-1 cells in vitro. Results: The expressed levels of midkine raised in the heart of mice and HL-1 cells by treating with LPS. The cardiac dysfunction of septic mice was deteriorated by midkine overexpression and was improved by midkine knockdown. The increases of inflammatory factors in the heart of mice induced by LPS were further enhanced by midkine overexpression and were attenuated by midkine knockdown. The increase of myocardial apoptosis in septic mice was worsened after midkine overexpression and was alleviated after midkine downregulation. The oxidative stress increase in the heart of septic mice was exacerbated by overexpression of midkine and was attenuated by downregulation of midkine. Conclusions: These results indicated that midkine exacerbated cardiac dysfunction via enhanced inflammation, apoptosis and oxidative stress. Targeting of midkine could improve cardiac dysfunction via attenuation of inflammation, apoptosis and oxidative stress.

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Section: Introductionmentioning

confidence: 99%

Midkine exacerbates inflammation, apoptosis and oxidative stress in heart of septic mice

Wei

Liu

et al. 2023

Preprint

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Tangeretin attenuates acute lung injury in septic mice by inhibiting ROS-mediated NLRP3 inflammasome activation via regulating PLK1/AMPK/DRP1 signaling axis

Liu,

Zhang,

You

et al. 2023

Inflamm. Res.

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Electroacupuncture at Zusanli Alleviates Sepsis by Regulating the TLR4-MyD88-NF-Kappa B Pathway and Diversity of Intestinal Flora

Zhan

Líu

Zheng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. Electroacupuncture (EA) at the Zusanli acupoint (ST36) has shown therapeutic potential for sepsis due to its ability to limit inflammation and to regulate gastrointestinal tract symptoms. However, the mechanisms contributing to the effects of EA at ST36 on sepsis and connections with the intestinal flora remain unclear. This study was designed to explore the effects of EA at ST36 on Toll-like receptor 4 signaling and the intestinal flora. Methods. ICR mice were randomly divided into 4 groups: control group, model group, EA group, and sham EA group. EA at ST36 was performed at 2.5 mA and 2 to 100 Hz, and the 30 min of dense wave was achieved over 5 days. A sepsis model was built by intraperitoneal injection of lipopolysaccharide (LPS, 10 mg/mL). The levels of expression of interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), and IL-10 were detected by enzyme-linked immunosorbent assays, and lactate dehydrogenase (LDH) levels in serum were measured by biochemical tests. Expression levels of Bax, Bcl2, cleaved caspase-3, Toll-like receptor (TLR4), nuclear factor-kappa B (NF-κB), and myeloid differentiation factor 88 (MyD88) were assessed by the Western blotting. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining was used to evaluate apoptosis. The intestinal microecology was assessed via 16S rRNA gene sequencing. Results. EA at ST36 reduced the expression of IL-1β, IL-6, and TNF-α and increased the expression of IL-10 to inhibit the inflammatory response. EA at ST36 also inhibited apoptosis, as measured by TUNEL staining, and decreased the Bax/Bcl2 ratio and levels of caspase-3 and cleaved caspase-3, as well as LDH release. Our results suggest that alleviation of sepsis may correlate with the downregulation of levels of TLR4, NF-κB, and MyD88. Importantly, EA at ST36 improved the diversity of the intestinal flora and increased the abundance of Firmicutes and Actinobacteria. Conclusion. EA at ST36 prevented sepsis from worsening by inhibiting inflammation and apoptosis, which correlated with the regulation of the TLR4/NF-κB/MyD88 signaling axis and modulation of the intestinal flora.

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Systemic inflammation and sepsis. Part II: Functional consequences of the storm

Cited by 3 publications

References 89 publications

Midkine exacerbates inflammation, apoptosis and oxidative stress in heart of septic mice

Midkine exacerbates inflammation, apoptosis and oxidative stress in heart of septic mice

Tangeretin attenuates acute lung injury in septic mice by inhibiting ROS-mediated NLRP3 inflammasome activation via regulating PLK1/AMPK/DRP1 signaling axis

Electroacupuncture at Zusanli Alleviates Sepsis by Regulating the TLR4-MyD88-NF-Kappa B Pathway and Diversity of Intestinal Flora

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