Anti-Inflammatory Pyranochalcone Derivative Attenuates LPS-Induced Acute Kidney Injury via Inhibiting TLR4/NF-κB Pathway

Shi, Min; Zeng, Xiaoxi; Guo, Fan; Huang, Rongshuang; Feng, Yanhuan; Ma, Liang; Zhou, Li; Fu, Ping

doi:10.3390/molecules22101683

Cited by 43 publications

(30 citation statements)

References 33 publications

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“…Wnt/β‐catenin and NF‐κB pathways have been verified to be involved in adjusting inflammation in heterogeneous illnesses. [ 36,37 ] A report showed that suppression of Wnt/β‐catenin could abate inflammation, meanwhile assuage sepsis‐engendered organ damage. [ 38 ] On the other hand, Chen et al [ 32 ] and Huang et al [ 39 ] have revealed that lncRNA NEAT1 and PVT1 affected LPS‐triggered septic AKI through regulation of the NF‐κB pathway.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HOXA‐AS2 mediates microRNA‐106b‐5p to repress sepsis‐engendered acute kidney injury

Wu¹,

Wang

2020

J Biochem & Molecular Tox

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HOXA cluster antisense RNA 2 (HOXA‐AS2) is a long noncoding RNA associated with the development of numerous cancers. But, whether HOXA‐AS2 exhibits a certain function in sepsis‐engendered acute kidney injury (AKI) remains uninvestigated. We strived to unveil the role of HOXA‐AS2 in sepsis‐engendered AKI. The expression of HOXA‐AS2 in sepsis patients, animal models and lipopolysaccharide (LPS)‐impaired HK‐2 cells was primarily assessed via a real‐time quantitative polymerase chain reaction. The effects of HOXA‐AS2 on cell survival of HK‐2 cells under LPS irritation were evaluated after overexpression of HOXA‐AS2. The correlation between HOXA‐AS2 and microRNA (miR)‐106b‐5p was forecasted via bioinformatics software and verified by using a luciferase report system. Subsequently, the functions of miR‐106b‐5p in LPS‐damaged HK‐2 cells were reassessed. Western blot was used for the determination of Wnt/β‐catenin and nuclear factor‐κB (NF‐κB) pathways. HOXA‐AS2 expression was decreased in sepsis patients, animal operation group and LPS‐irritated HK‐2 cells. Overexpressed HOXA‐AS2 mollified LPS‐triggered impairment in HK‐2 cells. In addition, a negative mediatory relation between HOXA‐AS2 and miR‐106b‐5p was predicated. Synchronously, overexpressed miR‐106b‐5p counteracted the protection of HOXA‐AS2 in LPS‐damaged HK‐2 cells. Ultimately, Wnt/β‐catenin and NF‐κB pathways were hindered by HOXA‐AS2 via targeting miR‐106b‐5p. HOXA‐AS2 exhibited protection in sepsis‐engendered AKI via targeting miR‐106b‐5p and hindering the Wnt/β‐catenin and NF‐κB pathways.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HOXA‐AS2 mediates microRNA‐106b‐5p to repress sepsis‐engendered acute kidney injury

Wu¹,

Wang

2020

J Biochem & Molecular Tox

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“…According to the preceding study reported by Shi et al [22], the kidney injury cell model was established by the treatment of 2 lg/mL LPS for 6 h towards HK-2 cells. Initially, we affirmed that LPS elicited cANRIL expression in HK-2 cells when compared to the without LPS group (p < .001, Figure 1(A)).…”

Section: Lps Elicited the Canril Expression In Hk-2 Cellsmentioning

confidence: 99%

Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9

Deng

Chen

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Circular antisense non-coding RNA in the INK4 locus (cANRIL) participated in inflammation of endothelial cells. However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL participated in inflammatory response in vitro. HK-2 cells were stimulated by lipopolysaccharides (LPS). RT-qPCR was executed for cANRIL expression assessment. After transfection, cell viability, apoptosis, inflammatory cytokines and ROS generation were appraised to evaluate the impact of silencing cANRIL on LPS-induced inflammatory injury. The regulatory relationship between cANRIL and microRNA-9 (miR-9) was verified. In addition, whether miR-9 affected LPS-induced inflammatory injury was measured after miR-9 inhibitor transfection. Western blot was utilized to detect NF-jB and JNK/p38 pathway-related proteins. The results showed that LPS promoted cANRIL expression and cell injuries in HK-2 cells. Furthermore, silencing cANRIL alleviated inflammatory injuries by promoting viability, suppressing apoptosis, inflammatory cytokines and ROS generation in HK-2 cells. In addition, miR-9 expression was accelerated by silencing cANRIL. Meanwhile, miR-9 down-regulation invalidated the effect of silencing cANRIL on inflammation and NF-jB and JNK/p38 pathways. The study clarified that silencing cANRIL hindered NF-jB and JNK/p38 pathways by positively regulating miR-9, thereby protecting HK-2 cells from LPS-induced injury.

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“…found that PTEN was up‐regulated in kidney tissue of septic rats and HK‐2 cells. Shi et al . observed that inhibition of TLR4/NF‐κB pathway could reduce inflammatory response and urine derived sepsis‐induced kidney injury.…”

Section: Introductionmentioning

confidence: 99%

“…[9] Fu et al [10] found that PTEN was up-regulated in kidney tissue of septic rats and HK-2 cells. Shi et al [11] observed that inhibition of TLR4/NF-jB pathway could reduce inflammatory response and urine derived sepsisinduced kidney injury. Lipopolysaccharide is a classical ligand for TLR4 that can activate TLR4-/NF-jB signaling pathway in acute kidney injury mice, which leads to the increase of inflammatory cytokine, such as interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a).…”

Section: Introductionmentioning

confidence: 99%

LncRNA TapSAKI promotes inflammation injury in HK-2 cells and urine derived sepsis-induced kidney injury

Shen

Liu

Zhang

et al. 2019

Journal of Pharmacy and Pharmacology

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Objective To explore the possible mechanism of lncRNA TapSAKI in urine derived sepsis‐induced kidney injury. Materials and methods In vivo urine‐derived sepsis (US) rat model and in vitro LPS‐induced HK‐2 cells were established, and TapSAKI, miR‐22, PTEN, TLR4 and p‐p65 expressions were detected by qRT‐PCR and western blot. RNA precipitation and RNA pull‐down were performed to confirm the interaction between TapSAKI and miR‐22. Results TapSAKI was up‐regulated, miR‐22 was down‐regulated, PTEN, TLR4 and p‐p65 expressions, and inflammatory factors TNF‐α and IL‐6 levels were up‐regulated in kidney tissue of US rats and LPS‐induced HK‐2 cells. In addition, TapSAKI interacted with miR‐22, and negatively modulate miR‐22 expression. We also observed TapSAKI promoted PTEN expression, TLR4/NF‐κB pathway related proteins TLR4 and p‐p65, and apoptosis protein cleaved‐caspase‐3 through negatively regulating miR‐22. Further experiments proved TapSAKI/miR‐22/TLR4/NF‐κB pathway could promote HK‐2 cell apoptosis. Finally, in vivo experiments showed TapSAKI knockdown negatively regulated miR‐22 and positively regulate PTEN, decreased renal function indicators blood urea nitrogen and serum creatinine, and reduced TNF‐α and IL‐6. Conclusion TapSAKI was elevated in urine derived sepsis‐induced kidney injury, and promoted HK‐2 cell apoptosis and inflammatory response through miR‐22/PTEN/TLR4/NF‐κB pathway.

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Anti-Inflammatory Pyranochalcone Derivative Attenuates LPS-Induced Acute Kidney Injury via Inhibiting TLR4/NF-κB Pathway

Cited by 43 publications

References 33 publications

Long noncoding RNA HOXA‐AS2 mediates microRNA‐106b‐5p to repress sepsis‐engendered acute kidney injury

Long noncoding RNA HOXA‐AS2 mediates microRNA‐106b‐5p to repress sepsis‐engendered acute kidney injury

Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9

LncRNA TapSAKI promotes inflammation injury in HK-2 cells and urine derived sepsis-induced kidney injury

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