Tanshinone II Aattenuates renal damage in STZ-induced diabetic rats via inhibiting oxidative stress and inflammation

Xia, Chen; Wu, Rui; Kong, Yiwei; Yang, Yuting; Gao, Yu; Sun, Dandan; QiZhen, Liu; Dai, Dongjun; Lu, Zeyuan; Wang, Niansong; Ge, Shengfang; Wang, Zhen

doi:10.18632/oncotarget.16651

Cited by 54 publications

(40 citation statements)

References 57 publications

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“…Albuminuria and increases in the indicated renal function parameters (Scr and BUN) are considered the hallmarks of progression in renal diseases (Chen & Liu, ). We detected Scr, BUN, 24‐hr urine and urinary protein excretion in the six groups, which were showed in Figure a–d.…”

Section: Resultsmentioning

confidence: 99%

Celastrol attenuates renal injury in diabetic rats via MAPK/NF‐κB pathway

Zhang

Cao

Yang

et al. 2019

Phytotherapy Research

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The purpose of this study was to investigate the renal protective effect of celastrol on diabetic rats. Furthermore, the mechanism of its action was discussed whether it was related to MAPK/NF-κB signaling pathway. There were a total of 36 rats. Six rats were randomly chosen as the control group. The remaining 30 rats were given 1% streptozotocin intraperitoneal injection (50 mg/kg) and were randomly divided into five groups: the model control group, the low-dose celastrol group, the high-dose celastrol group, the Tripterygium wilfordii polyglycosides group, and the MAPK/NF-κB inhibitor group. After 4 weeks of continuous administration, 24-hr urine volume, urinary protein, blood urea nitrogen, and serum creatinine content were observed, and hematoxylin-eosin (HE) staining of the kidney and liver were evaluated.

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Section: Resultsmentioning

confidence: 99%

Celastrol attenuates renal injury in diabetic rats via MAPK/NF‐κB pathway

Zhang

Cao

Yang

et al. 2019

Phytotherapy Research

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“…There are many circumstances in which it is medically necessary to utilize contrast-enhanced imaging, despite the significant risk of CIN. Oxidative stress and inflammation play an important role in the pathogenesis of many kidney injuries including CIN [27-30]. Contrast media induces ROS that causes lipid peroxidation and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA Attenuates Contrast-Induced Nephropathy via Nrf2 Activation in Rats

Liang

Zhao

Cheng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Tanshinone IIA is a chemical compound extracted from Salvia miltiorrhiza Bunge, a perennial plant also known as red sage used in traditional Chinese medicine. Tanshinone IIA has been shown to protect against various organ injuries. In this study, we hypothesized that Tanshinone IIA could play an anti-oxidative role in contrast-induced nephropathy (CIN) through enhancing Nrf2/ARE activation. Methods: To test whether Tanshinone IIA can attenuate CIN, oxidative stress, and apoptosis, we utilized two models: an in vivo Sprague-Dawley rat model of ioversol-induced CIN and an in vitro cell model of oxidative stress in which HK2 cells, a human renal tubular cell line, are treated with hydrogen peroxide (H₂O₂). Rats were randomly assigned to 4 groups (n = 6 per group): control group, ioversol group (ioversol-induced CIN), vehicle group (ioversol-induced CIN rats pretreated with vehicle), and Tanshinone IIA group (ioversol-induced CIN rats pretreated with 25mg/kg Tanshinone IIA). Renal functions, renal injuries and apoptosis were evaluated by using serum creatinine, histological scoring, and TUNEL staning respectively. Malondialdehyde, 8-hydroxy-2’ –deoxyguanosine, and intracellular reactive oxygen species were used for oxidative stress assessment. Levels of Nrf2 and heme oxygenase-1 (HO-1) were measured in vivo and in vitro. Results: Tanshinone IIA attenuated renal tubular necrosis, apoptosis and oxidative stress in rats and oxidative stress in HK2 cells. Furthermore, Tanshinone IIA activated Nrf2, and up-regulated HO-1 expression in vivo and in vitro, resulting in a reduction in oxidative stress. Conclusion: Tanshinone IIA may protect against CIN through enhancing Nrf2/ARE activation.

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“…In recent years, the correlation between SphK1 and DN has gradually become a hot topic, followed by an opinion that diabetic renal fibrotic disease is one kind of chronic inflammatory response in kidneys [ 5 , 46 ]. SphK1 is also involved in the activation of several inflammatory responses during the regulation of cell physiological activities.…”

Section: Discussionmentioning

confidence: 99%

“…However, the pathological mechanism of DN has not been fully elucidated. Increasing number of studies suggest that inflammation is involved in the development and progression of DN, and it even receives serious attention that diabetic renal fibrotic disease is one kind of renal chronic inflammatory response [ 5 – 7 ]. NF-κB, a classic inflammatory signaling pathway, regulates expressions of numerous genes regarding inflammatory response in the process of clinical and experimental kidney disease [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Sphingosine kinase 1 mediates diabetic renal fibrosis via NF-κB signaling pathway: involvement of CK2α

Huang

Chen

et al. 2017

Oncotarget

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Sphingosine kinase 1 (SphK1) plays a pivotal role in regulating diabetic renal fibrotic factors such as fibronectin (FN) and intercellular adhesion molecule-1 (ICAM-1). Especially, activation of SphK1 is closely linked to the body inflammatory reaction. Casein kinase 2α subunit (CK2α), a protein kinase related to inflammatory reaction, influences diabetic renal fibrosis and expressions of FN and ICAM-1 via NF-κB pathway. However, the mechanism by which SphK1 mediates diabetic renal fibrosis has not yet fully elucidated. The current study is aimed to investigate if SphK1 mediates diabetic renal fibrotic pathological process via inflammatory pathway and activation of CK2α. The following findings were observed: (1) Expressions of SphK1 were upregulated in kidneys of diabetic mice and rats; (2) Knockdown of SphK1 expression suppressed high glucose (HG)-induced NF-κB nuclear translocation and expressions of FN and ICAM-1; (3) Compared with C57 diabetic mice, SphK1-/- diabetic mice exhibited less renal fibrotic lesions, FN accumulation and NF-κB nuclear accumulation in glomeruli of kidneys; (4) SphK1 mediated phosphorylation of CK2α, while CK2α knockdown depressed SphK1-induced activation of NF-κB pathway. This study indicates the essential role of SphK1 in regulating activation of CK2α and diabetic renal fibrotic pathological process via NF-κB.

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Tanshinone II Aattenuates renal damage in STZ-induced diabetic rats via inhibiting oxidative stress and inflammation

Cited by 54 publications

References 57 publications

Celastrol attenuates renal injury in diabetic rats via MAPK/NF‐κB pathway

Celastrol attenuates renal injury in diabetic rats via MAPK/NF‐κB pathway

Tanshinone IIA Attenuates Contrast-Induced Nephropathy via Nrf2 Activation in Rats

Sphingosine kinase 1 mediates diabetic renal fibrosis via NF-κB signaling pathway: involvement of CK2α

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