Clinical significance of sirtuin 1 level in sepsis: correlation with disease risk, severity, and mortality risk

Cheng, Xiao; Zhang, Senbing; Wen, Yan; Shi, Zhenzhong

doi:10.1590/1414-431x202010271

Cited by 4 publications

(1 citation statement)

References 19 publications

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“…[12][13][14][15] It has been implicated to attenuate sepsis-associated organ injury including SI-AKI. 16,17 SIRT1 is widely expressed in various tissues, while SIRT1 mainly exists in mesangial cells and epithelial cells of renal tubules in the kidney. 18 In vitro experiments show that SIRT1 can be used in the protection of kidney injury induced by oxidant, cisplatin, and ischemia-reperfusion through antioxidant stress, mitochondrial regeneration, and inhibition of apoptosis.…”

Section: Western Blotting Assaymentioning

confidence: 99%

Sevoflurane ameliorates LPS-induced inflammatory injury of HK-2 cells through Sirtuin1/NF-κB pathway

Wang

Yin

et al. 2022

Allergol Immunopathol

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The anesthetic sevoflurane (SEV) has been shown to protect against organ’s injury during sepsis. The present study intended to uncover the protective effects of SEV on sepsis-induced acute kidney injury (SI-AKI) and its possible mechanism. Human renal tubular epithelial cell HK-2 was treated with 10 μg/mL lipopolysaccharide (LPS) to construct SI-AKI cell model. LPS-induced HK-2 cells were pretreated with SEV in the absence or presence of EX527, an inhibitor of Sirtuin 1 (SIRT1), after which were the detection of cell viability, lactate dehydrogenase (LDH) release, apoptosis, inflammation, and oxidative stress. Our results demonstrated that LPS caused decreased cell viability, increased LDH release, improved cell apoptosis along with decreased expression of Bcl2 and enhanced expressions of Bax, cleaved PARP and cleaved caspase, enhanced production, and protein expressions of TNF-α, IL-6, and IL-1β, increased generation of reactive oxygen species (ROS) and malondialdehyde (MDA), but contributed to declined activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). LPS inhibited SIRT1 and IκBα expressions but upregulated p-NF-κB p65 and acetyl-p53 expressions as well. However, SEV pretreatment abolished all above-mentioned effects of LPS on HK-2 cells, while EX527 significantly reversed the effects of SEV. In conclusion, SEV effectively protected HK-2 cells against LPS-induced apoptosis, inflammation, and oxidative stress, and these effects may depend on the increase of SIRT1 expression, thereby inactivating NF-κB signaling.

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Section: Western Blotting Assaymentioning

confidence: 99%

Sevoflurane ameliorates LPS-induced inflammatory injury of HK-2 cells through Sirtuin1/NF-κB pathway

Wang

Yin

et al. 2022

Allergol Immunopathol

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An ultra-sensitive electrochemical biosensor for the detection of procalcitonin in sepsis patients’ serum, using a Cu-BHT-based thin film

Guo,

Yan,

et al. 2024

Talanta

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Inflammatory liver diseases and susceptibility to sepsis

2024

Clinical Science

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Patients with inflammatory liver diseases, particularly alcohol-associated liver disease and metabolic dysfunction-associated fatty liver disease (MAFLD), have higher incidence of infections and mortality rate due to sepsis. The current focus in the development of drugs for MAFLD is the resolution of non-alcoholic steatohepatitis and prevention of progression to cirrhosis. In patients with cirrhosis or alcoholic hepatitis, sepsis is a major cause of death. As the metabolic center and a key immune tissue, liver is the guardian, modifier, and target of sepsis. Septic patients with liver dysfunction have the highest mortality rate compared with other organ dysfunctions. In addition to maintaining metabolic homeostasis, the liver produces and secretes hepatokines and acute phase proteins (APPs) essential in tissue protection, immunomodulation, and coagulation. Inflammatory liver diseases cause profound metabolic disorder and impairment of energy metabolism, liver regeneration, and production/secretion of APPs and hepatokines. Herein, the author reviews the roles of (1) disorders in the metabolism of glucose, fatty acids, ketone bodies, and amino acids as well as the clearance of ammonia and lactate in the pathogenesis of inflammatory liver diseases and sepsis; (2) cytokines/chemokines in inflammatory liver diseases and sepsis; (3) APPs and hepatokines in the protection against tissue injury and infections; and (4) major nuclear receptors/signaling pathways underlying the metabolic disorders and tissue injuries as well as the major drug targets for inflammatory liver diseases and sepsis. Approaches that focus on the liver dysfunction and regeneration will not only treat inflammatory liver diseases but also prevent the development of severe infections and sepsis.

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Clinical significance of sirtuin 1 level in sepsis: correlation with disease risk, severity, and mortality risk

Cited by 4 publications

References 19 publications

Sevoflurane ameliorates LPS-induced inflammatory injury of HK-2 cells through Sirtuin1/NF-κB pathway

Sevoflurane ameliorates LPS-induced inflammatory injury of HK-2 cells through Sirtuin1/NF-κB pathway

An ultra-sensitive electrochemical biosensor for the detection of procalcitonin in sepsis patients’ serum, using a Cu-BHT-based thin film

Inflammatory liver diseases and susceptibility to sepsis

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