Erythropoietin promotes energy metabolism to improve LPS-induced injury in HK-2 cells via SIRT1/PGC1-α pathway

Li, Kan; Li, Gao; Zhou, Sen; Yue, Ma; Xiao, Xiao; Jiang, Qian; Kang, Zhihong; Liu, Ming-Long; Liu, Tian-Xi

doi:10.1007/s11010-022-04540-y

Cited by 10 publications

(6 citation statements)

References 51 publications

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“…Furthermore, LPS treatment can cause pathological damage, leading to a decrease in adenosine triphosphate (ATP) production compared to untreated cells. 34 Fortunately, the addition of CeLutNCs also recovered the production of ATP (Figure 4g). Together, these findings collectively demonstrate the effective antioxidative capability of CeLutNCs and their ability to provide cell protection.…”

Section: Resultsmentioning

confidence: 86%

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Cerium–Luteolin Nanocomplexes in Managing Inflammation-Related Diseases by Antioxidant and Immunoregulation

Gu,

Zhang,

et al. 2024

ACS Nano

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Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and the antioxidant defense system, plays a pivotal role in inflammationrelated diseases. Excessive ROS levels can induce cellular damage and impair normal physiological functions, triggering the release of inflammatory mediators and exacerbating the inflammatory response, ultimately leading to irreversible tissue damage. In this study, we synthesized cerium ion−luteolin nanocomplexes (CeLutNCs) by coordinating Ce ions with the natural product luteolin, aiming to develop a therapeutic agent with excellent antioxidant and immunoregulation properties for ROS-related inflammation treatment. In vitro experiments demonstrated that the prepared CeLutNCs effectively scavenged excess ROS, prevented cell apoptosis, downregulated levels of important inflammatory cytokines, regulated the response of inflammatory macrophages, and suppressed the activation of the nuclear factor-κ-gene binding (NF-κB) pathway. In an acute kidney injury (AKI) animal model, CeLutNCs exhibited significant efficacy in improving kidney function, repairing damaged renal tissue, and reducing oxidative stress, inflammatory response, and cellular apoptosis. Moreover, the therapeutic potential of CeLutNCs in an acute lung injury (ALI) model was confirmed through the assessment of inflammatory responses and histopathological studies. This study emphasizes the effectiveness of these metal−natural product coordination nanocomplexes as a promising therapeutic approach for preventing AKI and other diseases associated with oxidative stress.

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Section: Resultsmentioning

confidence: 86%

“…Similar results were observed in NRK-52E cells (Figure S14). Furthermore, LPS treatment can cause pathological damage, leading to a decrease in adenosine triphosphate (ATP) production compared to untreated cells . Fortunately, the addition of CeLutNCs also recovered the production of ATP (Figure g).…”

Section: Results and Discussionmentioning

confidence: 99%

Cerium–Luteolin Nanocomplexes in Managing Inflammation-Related Diseases by Antioxidant and Immunoregulation

Gu,

Zhang,

et al. 2024

ACS Nano

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“… 19 LPS can promote inflammation by inhibiting SIRT1 expression in kidney tissue. 20 Specific agonists of SIRT1 can antagonize LPS, reduce the release of inflammatory factors, alleviate tissue damage, and slow fibrosis progression. 21 In this study, IHC results showed that the expression of SIRT1 protein decreased in CHN-affected kidney tissue, and in vitro cell experiments showed that LPS inhibited SIRT1 expression in HK-2 cells, and the SIRT1-specific agonist SRT1720 could antagonize the inhibitory effect of LPS.…”

Section: Discussionmentioning

confidence: 99%

Role and significance of SIRT1 in regulating the LPS-activated pyroptosis pathway in children with congenital hydronephrosis

Wang,

Weizhong,

Zhou

et al. 2023

World Jnl Ped Surgery

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ObjectiveTo explore the characteristics and mechanism of sirtuin 1 (SIRT1) in lipopolysaccharide (LPS)-activated pyroptosis in the renal tissue of children with congenital hydronephrosis (CHn).MethodsWe detected the expression characteristics and clinical significance of SIRT1 and pyroptosis pathway proteins in CHn renal tissues by immunohistochemistry. The degree of renal fibrosis was detected by Masson staining. The human renal tubular epithelial cell line (HK-2) was cultured in vitro and treated with LPS (1 µg/mL), the SIRT1-specific agonist SRT1720 (2.5 µmol/L) and small interfering RNA (siRNA)-SIRT1 for 48 hours. After 48 hours, Cell Counting Kit-8 was used to detect the changes in cell proliferation ability, and ELISA was used to detect the changes in the expression of interleukin (IL)-1β and IL-18 in the cell supernatant. Real-time PCR (quantitative RT-PCR) and western blot analysis were used to detect the expression of SIRT1, caspase-1, caspase-4, NOD-like receptor thermal protein domain associated protein 3(NLRP3), and cleaved gasdermin D (GSDMD) in each group.ResultsSerum inflammatory cytokines were significantly elevated in 13 children with CHn with urinary tract infection, mainly caused by Gram-negative bacteria. Severe renal fibrosis occurred in children with CHn. Compared with the control group, the expression of SIRT1 in CHn kidney tissues was decreased, and the expression of caspase-4 and GSDMD was increased. LPS inhibited the expression of SIRT1 in HK-2 cells, promoted the expression of caspase-1, caspase-4, NLRP3, cleaved GSDMD, promoted the expression of IL-1β and IL-18 in the supernatant, and promoted pyroptosis in HK-2 cells. SRT1720 can inhibit LPS-activated pyroptosis by promoting SIRT1 expression, while siRNA-SIRT1 can further aggravate LPS-activated pyroptosis after inhibiting SIRT1 expression.ConclusionsLPS can promote the inflammatory response in children with CHn by activating non-canonical pyroptosis and inhibiting SIRT1 expression. Promoting SIRT1 expression can inhibit pyroptosis of renal tubular epithelial cells, reduce the release of IL-18 and IL-1β, and alleviate the progression of renal fibrosis in children with CHn.

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“…Conversely, early initiation of mitochondrial biogenesis and prompt response to oxidative stress are associated with higher survival rates in patients with critical illnesses (Carré et al, 2010). Promoting biogenesis through diverse strategies in septic mouse models has proven effective in preserving renal function and improving survival outcomes (Jin et al, 2020;Li et al, 2023). Furthermore, in vitro analyses demonstrate that the NRF2 pathway enhances mitophagy in renal cells and tubules, stimulates mitochondrial biogenesis under septic conditions, increases the abundance of functional mitochondria, and promotes a more robust mitochondrial network, which collectively mitigate inflammation, oxidative…”

Section: Building Resilience: Exploring Tecs' Resistance and Toleranc...mentioning

confidence: 99%

“…During SA-AKI, a notable decline in PGC-1α expression impairs energy production, underscoring the significance of PGC-1α (Tran et al, 2011;Smith et al, 2015). Therefore, enhancing PGC-1α levels-possibly through the administration of recombinant human erythropoietin (rhEPO) or by pharmacologically stimulating the AMPK pathway-may help mitigate the detrimental effects of sepsis (Cantó and Auwerx, 2009;Jin et al, 2020;Li et al, 2023).…”

Section: Restoring Oxphos: Rebalancing Tecs' Metabolismmentioning

confidence: 99%

Advances in metabolic reprogramming of renal tubular epithelial cells in sepsis-associated acute kidney injury

Wang,

Huang,

Zhang

et al. 2024

Front. Physiol.

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Sepsis-associated acute kidney injury presents as a critical condition characterized by prolonged hospital stays, elevated mortality rates, and an increased likelihood of transition to chronic kidney disease. Sepsis-associated acute kidney injury suppresses fatty acid oxidation and oxidative phosphorylation in the mitochondria of renal tubular epithelial cells, thus favoring a metabolic shift towards glycolysis for energy production. This shift acts as a protective mechanism for the kidneys. However, an extended reliance on glycolysis may contribute to tubular atrophy, fibrosis, and subsequent chronic kidney disease progression. Metabolic reprogramming interventions have emerged as prospective strategies to counteract sepsis-associated acute kidney injury by restoring normal metabolic function, offering potential therapeutic and preventive modalities. This review delves into the metabolic alterations of tubular epithelial cells associated with sepsis-associated acute kidney injury, stressing the importance of metabolic reprogramming for the immune response and the urgency of metabolic normalization. We present various intervention targets that could facilitate the recovery of oxidative phosphorylation-centric metabolism. These novel insights and strategies aim to transform the clinical prevention and treatment landscape of sepsis-associated acute kidney injury, with a focus on metabolic mechanisms. This investigation could provide valuable insights for clinicians aiming to enhance patient outcomes in the context of sepsis-associated acute kidney injury.

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Erythropoietin promotes energy metabolism to improve LPS-induced injury in HK-2 cells via SIRT1/PGC1-α pathway

Cited by 10 publications

References 51 publications

Cerium–Luteolin Nanocomplexes in Managing Inflammation-Related Diseases by Antioxidant and Immunoregulation

Cerium–Luteolin Nanocomplexes in Managing Inflammation-Related Diseases by Antioxidant and Immunoregulation

Role and significance of SIRT1 in regulating the LPS-activated pyroptosis pathway in children with congenital hydronephrosis

Advances in metabolic reprogramming of renal tubular epithelial cells in sepsis-associated acute kidney injury

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