Organellophagy regulates cell death:A potential therapeutic target for inflammatory diseases.

Background: Dysregulated alterations in organelle structure and function have a significant connection with cell death, as well as the occurrence and development of inflammatory diseases. Maintaining cell viability and inhibiting the release of inflammatory cytokines are essential measures to treat inflammatory diseases. Recently, many studies have showed that autophagy selectively targets dysfunctional organelles, thereby sustaining the functional stability of organelles, alleviating the release of multiple cytokines, and maintaining organismal homeostasis.

LncRNA GAS5 inhibits miR-579-3p to activate SIRT1/PGC-1α/Nrf2 signaling pathway to reduce cell pyroptosis in sepsis-associated renal injury.

Sepsis is a life-threatening condition that can lead to several organ failures including kidney. In this study, we investigated the roles of GAS5 and miR-579-3p in regulating cell pyroptosis in the sepsis-induced renal injury model. Lipopolysaccharide (LPS) treatment or cecal ligation and puncture (CLP) surgery was used to create the in vitro and in vivo sepsis-induced renal injury model.

The interaction between C/EBPβ and TFAM promotes acute kidney injury via regulating NLRP3 inflammasome-mediated pyroptosis.

Sepsis-induced inflammatory damage is a crucial cause of acute kidney injury (AKI), and AKI is an ecumenical fearful complication in approximately half of patients with sepsis. CCAAT/enhancer-binding protein β (C/EBPβ) plays roles in regulating acute phase responses and inflammation. However, the role and mechanism of C/EBPβ in AKI are unclear.

Involvement of phosphatase and tensin homolog-induced putative kinase 1-Parkin-mediated mitophagy in septic acute kidney injury.

Background: Studies have reported mitophagy activation in renal tubular epithelial cells (RTECs) in acute kidney injury (AKI). Phosphatase and tensin homolog-induced putative kinase 1 (PINK1) and E3 ubiquitin-protein ligase Parkin are involved in mitophagy regulation; however, little is known about the role of PINK1-Parkin mitophagy in septic AKI. Here we investigated whether the PINK1-Parkin mitophagy pathway is involved in septic AKI and its effects on cell apoptosis in vitro and on renal functions in vivo.

Upregulation of Mitochondrial Transcription Factor A Promotes the Repairment of Renal Tubular Epithelial Cells in Sepsis by Inhibiting Reactive Oxygen Species-Mediated Toll-Like Receptor 4/p38MAPK Signaling.

Background: Mitochondrial transcription factor A (TFAM) plays multiple pathophysiologic roles in mitochondrial DNA (mtDNA) maintenance. However, the role of TFAM in sepsis-induced acute kidney injury (AKI) remains largely unknown.

Methods: Lipopolysaccharide (LPS) treatment of HK-2 cells mimics the in vitro model of AKI inflammation.

[The experiment study of treatment of infectious acute lung injury by intravenous administration of adenovirus borne inhibitor of nuclear factor-ΚB gene in rat].

Objective: To observe the effects of adenovirus borne IΚB gene, an inhibitor of nuclear factor-ΚB (NF-ΚB), infused via central vein, to treat infectious acute lung injury (ALI) in rats.

Methods: According to random number table method, 30 pathogen-free Sprague-Dawley (SD) rats were randomly divided into three groups: sham group, ALI model group, IΚB gene treatment group, with 10 rats in each group. The rats of IΚB gene treatment group were infused 1 ml adenovirus borne IΚB gene (titre: 1×10(9)pfu ), the rats of sham group and ALI model group were infused 1 ml normal saline through central vein.

[The enhancing effect of "Xuebijing injection" on lipopolysaccharide-induced apoptosis of regulatory T cells and mediation of polarization of helper T cells].

Objective: To investigate the enhancing effect of Chinese medicine-Xuebijing injection on lipopolysaccharide (LPS) -induced apoptosis of CD4+ CD25+ regulatory T cells (Tregs) and polarization of helper T cells (Th).

Methods: CD4+ CD25+ Tregs collected from rat spleen in vitro by immunomagnetic beads assay were divided into the control group, anti-CD3/CD28 group, anti-CD3/CD28 + LPS group, anti-CD3/CD28 + "Xuebijing injection" group and anti-CD3/CD28 + LPS + "Xuebijing injection" group. Tregs apoptosis rate and expression of winged helix transcription factor (Foxp3) in Tregs were detected by flow cytometry on 3rd post culture day.

[Effect of apoptosis of CD4+ CD25+ regulatory T cells on proliferation as well as secretion of effector T cells and interventional activity of Xuebijing injection in septic rats].

Objective: To investigate the effect of apoptosis of CD4+ CD25+ regulatory T cells (Tregs) on proliferation as well as secretory function of effector T cells (Teff) and potential influence of Xuebijing injection on them in septic rats.

Methods: A sepsis model was reproduced by cecal ligation puncture (CLP), and Wistar rats were randomly divided into the control group (n = 8), sham-operated group (n = 8), CLP group (n = 8), and Xuebijing injection treatment group (n = 8). CD4+ CD25+ Tregs in each group were separated by immunomagnetic beads isolate system on day 3, the apoptosis rate, expression of forkhead/winged helix transcription factor p3 (Foxp3) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) on Tregs were analyzed by flow cytometry, and secretion levels of interleukin (IL)-10 from Tregs were measured by ELISA.

[Effect of apoptosis of CD4+ CD25+ regulatory T lymphocytes on polarization of helper T lymphocytes and potential interventional influence of Xuebijing injection in septic rats].

Objective: To evaluate the influence of apoptosis of CD4(+)CD25(+) regulatory T lymphocyte (Treg) on polarization of helper T lymphocyte (Th) and effect of Xuebijing injection in septic rats.

Methods: A sepsis model was reproduced by cecal ligation and puncture (CLP). Wistar rats were randomly divided into the normal group (n=8), sham operation group (n=8), model group (n=8) and Xuebijing injection treatment group (n=8).

[Research advances in Th17 cells].

CD4+ T cells have been divided into different subsets, essentially based on the cytokines they produce. These subsets include T helper cell (Th)1, Th2 and regulatory T cells (Treg). Recently, another subpopulation of T cells has been identified, and it was named as Th17, which is characterized by the release of interleukin (IL)-17.