The renoprotective effect of curcumin against cisplatin-induced acute kidney injury in mice: involvement of miR-181a/PTEN axis

Huang, Sijia; Huang, Jing; Yan, Yun-Bo; Qiu, Jiao; Tan, Rui-Qiao; Liu, Yu; Tian, Qing; Guan, Li; Niu, Sheng; Zhang, Yanxiang; Zhang, Xi; Xiang, Ying; Gong, Quan

doi:10.1080/0886022x.2020.1751658

Cited by 29 publications

(12 citation statements)

References 32 publications

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“…According to previous studies, cell apoptosis and inflammatory damage are the primary mechanisms by which cisplatin induces AKI (32)(33)(34). Some traditional Chinese medicines, which possess anti-inflammatory or anti-apoptotic effects have been shown to protect against kidney injury induced by cisplatin (35,36). GBE is extracted from ginkgo biloba leaves, which is a traditional Chinese natural herb and has a long history of clinical use for treatment of cardiovascular and cerebrovascular diseases (37).…”

Section: Discussionmentioning

confidence: 99%

Ginaton injection alleviates cisplatin‑induced renal interstitial fibrosis in rats via inhibition of apoptosis through regulation of the p38MAPK/TGF‑β1 and p38MAPK/HIF‑1α pathways

Liang

Wei

et al. 2021

Biomed Rep

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Ginaton injection (Ginkgo biloba extract; GBE) has been reported to protect against cisplatin-induced acute renal failure in rats. In the present study, the effects and molecular mechanisms of GBE on cisplatin-induced renal interstitial fibrosis were evaluated using a rat model. The rats were intraperitoneally injected with cisplatin once on the first day and a subset of rats were treated with GBE or SB203580 (SB; a specific p38 MAPK inhibitor) daily from days 22 to 40. The levels of N-acetyl-β-D-Glucosaminidase (NAG) in the urine, and of urea nitrogen (BUN) and creatinine (Scr) in the blood were assessed. The damage and fibrosis of renal tissues were evaluated using hematoxylin and eosin staining, as well as Masson's trichrome staining, respectively. Apoptosis in renal tissues was detected using a TUNEL assay. The protein expression levels of α-smooth muscle actin (SMA), collagen 1 (Col I), Bax, Bcl-2, caspase-3/cleaved caspase-3, hypoxia-inducible factor-1α (HIF-1α), TGF-β1 and p38MAPK, as well as the mRNA levels of p38MAPK in renal tissues were investigated. The results showed that GBE markedly reduced the levels of urinary NAG, Scr and BUN, and renal expression of α-SMA and Col I levels were also reduced. Furthermore, GBE significantly reduced renal tissue injury and the relative area of renal interstitial fibrosis induced by cisplatin. GBE effectively reduced the apoptotic rate of renal tissues, the protein expression levels of Bax, cleaved caspase-3, phospho-p38MAPK, TGF-β1 and HIF-1α, as well as the mRNA expression levels of p38MAPK in renal tissues induced by cisplatin, whereas GBE significantly increased Bcl-2 protein expression. SB exhibited similar effects to GBE, although it was not as effective. In summary, the present study is the first to show that GBE significantly alleviated renal interstitial fibrosis following cisplatin-induced acute renal injury. The mechanisms by which GBE exhibited its effects were associated with the inhibition of apoptosis via downregulation of the p38MAPK/TGF-β1 and p38MAPK/HIF-1α signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Ginaton injection alleviates cisplatin‑induced renal interstitial fibrosis in rats via inhibition of apoptosis through regulation of the p38MAPK/TGF‑β1 and p38MAPK/HIF‑1α pathways

Liang

Wei

et al. 2021

Biomed Rep

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“…All studies were published in English, between 2010 and 2021. Most of these studies were conducted in China [24,25,31,32,[36][37][38][39][40][41][42][43][44][47][48][49][50] and the United States of America (USA) [26,27,34,38,46]. The main differences among the 30 included studies were related All studies were published in English, between 2010 and 2021.…”

Section: Resultsmentioning

confidence: 99%

“…Of the remaining 432 articles, 393 were excluded by reviewing their titles and abstracts. The full text of the remaining 39 articles underwent a review, and 30 studies [ 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 ] that met the eligibility criteria were included. Figure 1 shows a flowchart of the literature search and Supplementary Table S1 .…”

Section: Resultsmentioning

confidence: 99%

“…All studies were published in English, between 2010 and 2021. Most of these studies were conducted in China [ 24 , 25 , 31 , 32 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 47 , 48 , 49 , 50 ] and the United States of America (USA) [ 26 , 27 , 34 , 38 , 46 ]. The main differences among the 30 included studies were related to population, cisplatin dose, nephrotoxicity assessment, and time of analysis of the miRNAs.…”

Section: Resultsmentioning

confidence: 99%

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Dysregulated MicroRNAs as Biomarkers or Therapeutic Targets in Cisplatin-Induced Nephrotoxicity: A Systematic Review

Torso

Pereira

Visacri

et al. 2021

IJMS

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The purpose of this systematic review was to map out and summarize scientific evidence on dysregulated microRNAs (miRNAs) that can be possible biomarkers or therapeutic targets for cisplatin nephrotoxicity and have already been tested in humans, animals, or cells. In addition, an in silico analysis of the two miRNAs found to be dysregulated in the majority of studies was performed. A literature search was performed using eight databases for studies published up to 4 July 2021. Two independent reviewers selected the studies and extracted the data; disagreements were resolved by a third and fourth reviewers. A total of 1002 records were identified, of which 30 met the eligibility criteria. All studies were published in English and reported between 2010 and 2021. The main findings were as follows: (a) miR-34a and miR-21 were the main miRNAs identified by the studies as possible biomarkers and therapeutic targets of cisplatin nephrotoxicity; (b) the in silico analysis revealed 124 and 131 different strongly validated targets for miR-34a and miR-21, respectively; and (c) studies in humans remain scarce.

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“…MiRs bind to target genes to regulate the inflammatory response, apoptosis, and cell cycle during the damage and repair stage after AKI, and play a corresponding role in the transition to CKD. For example, miR-27a-3p, miR-205, miR-17-5p, miR-126, and miR-688 can inhibit the conversion of AKI to CKD by improving renal function, reducing fibrosis and inflammatory response [73,[78][79][80][81]; on the contrary, miR-24, miR-494, miR-150, miR-181a, and miR-687 can promote this process [82][83][84][85][86]. miR-21 is a "double-edged sword," with mild upregulation inhibiting fibrosis and inflammatory response but sustained upregulation promoting tubulointerstitial fibrosis after AKI [87].…”

Section: Noncoding Rnasmentioning

confidence: 99%

Epigenetic Modification Drives Acute Kidney Injury-to-Chronic Kidney Disease Progression

2021

Nephron

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Acute kidney injury (AKI) is a common clinical critical disease. Due to its high morbidity, increasing risk of complications, high mortality rate, and high medical costs, it has become a global concern for human health problems. Initially, researchers believed that kidneys have a strong ability to regenerate and repair, but studies over the past 20 years have found that kidneys damaged by AKI are often incomplete or even unable to repair. Even when serum creatinine returns to baseline levels, renal structural damage persists for a long time, leading to the development of chronic kidney disease (CKD). The mechanism of AKI-to-CKD transition has not been fully elucidated. As an important regulator of gene expression, epigenetic modifications, such as histone modification, DNA methylation, and noncoding RNAs, may play an important role in this process. Alterations in epigenetic modification are induced by hypoxia, thus promoting the expression of inflammatory factor-related genes and collagen secretion. This review elaborated the role of epigenetic modifications in AKI-to-CKD progression, the diagnostic value of epigenetic modifications biomarkers in AKI chronic outcome, and the potential role of targeting epigenetic modifications in the prevention and treatment of AKI to CKD, in order to provide ideas for the subsequent establishment of targeted therapeutic strategies to prevent the progression of renal tubular-interstitial fibrosis.

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The renoprotective effect of curcumin against cisplatin-induced acute kidney injury in mice: involvement of miR-181a/PTEN axis

Cited by 29 publications

References 32 publications

Ginaton injection alleviates cisplatin‑induced renal interstitial fibrosis in rats via inhibition of apoptosis through regulation of the p38MAPK/TGF‑β1 and p38MAPK/HIF‑1α pathways

Ginaton injection alleviates cisplatin‑induced renal interstitial fibrosis in rats via inhibition of apoptosis through regulation of the p38MAPK/TGF‑β1 and p38MAPK/HIF‑1α pathways

Dysregulated MicroRNAs as Biomarkers or Therapeutic Targets in Cisplatin-Induced Nephrotoxicity: A Systematic Review

Epigenetic Modification Drives Acute Kidney Injury-to-Chronic Kidney Disease Progression

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