Aloe-Emodin Ameliorates Renal Fibrosis Via Inhibiting PI3K/Akt/mTOR Signaling PathwayIn VivoandIn Vitro

Dou, Fang; Liu, Yuetong; Liu, Limin; Wang, Jingwen; Sun, Ting; Mu, Fei; Guo, Qiyan; Guo, Chao; Jia, Na; Liu, Wenxin; Ding, Yi; Wen, Aidong

doi:10.1089/rej.2018.2104

Cited by 83 publications

(54 citation statements)

References 46 publications

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“…A critical downstream mediator of PI3K is AKT, which acts on a number of different targets that affect cellular survival, activation of transcription/translation, apoptosis and proliferation through resistance to chemotherapy. Upstream regulation of mTOR with a downstream target of AKT and a serine/threonine kinase leads to activation of proteins that directly affect protein translation and growth progression through the cell cycle [3]. In this study, we aimed to demonstrate the effect of cyclophosphamide on PI3K/AKT/mTOR signaling pathway in kidney tissue.…”

Section: Introductionmentioning

confidence: 99%

Cyclophosphamide Inhibits PI3K/AKT/mTOR Signaling Pathway in Mice Kidneys

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Akoğulları

et al. 2018

The 2nd International Cell Death Research Congress

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Cyclophosphamide (CTX), also known as cytophosphane among other, is a medication used as chemotherapy and to suppress the immune system. The PI3K/AKT/mTOR pathway is involved in the regulation of diverse cellular functions, including cell growth, protein synthesis, cell cycle regulation, glucose metabolism, and motility. In our study eight weeks old C57BL/6 female mice were divided into 3 groups as control (C), sham (S) and experimental group. The experimental group has been established with CTX treatment. No treatment was applied to the C group. The S group were given an equal amount of saline. CTX was administered intraperitoneally one every 2 days for 3 weeks; the first dose was 70 mg/kg, the ongoing doses were 30 mg/kg. At the end of 3 weeks mice were sacrificed and kidneys were taken for investigation. In order to show the effect of cyclophosphamide in kidney tissue, the tissues were stained via indirect immunohistochemistry with PI3K, AKT and mTOR primary antibodies. In our study, PI3K, AKT and mTOR expression levels were found to be significantly decreased in CTX-mediated mechanisms indicating that the mechanisms of CTX might involve in the inhibition of PI3K/AKT/mTOR signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Cyclophosphamide Inhibits PI3K/AKT/mTOR Signaling Pathway in Mice Kidneys

Albayrak

Sonmez

Akoğulları

et al. 2018

The 2nd International Cell Death Research Congress

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“…Meanwhile, a series of compounds exhibited an effect on cataract by modulating the PI3K-Akt signaling pathway, such as alkylphosphocholine erufosine [58], quercetin [59], and andrographolide [60]. Many of the active ingredients in CS have been proven to regulate the PI3K-Akt signaling pathway, including rhein [16], aloe-emodin [61], and rubrofusarin [62], indicating that CS acted on cataracts possibly through the PI3K-Akt signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Exploring the Pharmacological Mechanism of Cassiae Semen a Cting on Cataracts Based on a Network Pharmacology Approach

Fang¹

2020

Preprint

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BackgroundCassiae Semen (CS) is one of the most well-known herbs used in the treatment of cataracts in China. However, the potential mechanisms of its anti-cataracts effects have not been fully explored.MethodThe active compounds of CS were obtained from TCMSP database, and their targets were retrieved from the TCMSP, STITCH and DrugBank databases. Cataracts related target genes were identified from the GeneCard, Malacard, and OMIM databases. GO and KEGG analysis were performed using DAVID online tools, and Cytoscape were used to construct compound-targets network and protein-protein interaction (PPI) networks, cluster analysis were carried out using MCODE plugin for Cytoscape.ResultsWe obtained 13 active compounds from CS and 105 targets in total to construct a compound-target network, which indicated that emodin, stigmastero, and rhein served as the main ingredients in CS. A total of 238 cataracts related targets were identified from public databases. PPI networks of compound targets and cataract-related targets were constructed and merged to obtained the central network, enrichment analysis showed 50 key targets in the central network enriched in several important signaling pathways, such as thyroid hormone signaling pathway, MAPK signaling pathway, PI3K-Akt signaling pathway. The top 4 genes with higher degree in the central network were TP53, HSP90, ESR1, EGFR, indicating their important roles in the treatment of cataracts.ConclusionsThe present study systematically revealed the multi-target mechanisms of CS on cataracts using network pharmacology approach, and provided indications for further mechanistic studies and also for the development of CS as a potential treatment for cataracts patients.

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“…14,15 Additionally, it has previously been verified that emodin can relieve the progression of renal fibrosis. 16 However, the antifibrotic effect of emodin in combination with HGF has not been confirmed yet. TGFβ participates in many cellular processes, including cell growth, differentiation, apoptosis, and homeostasis.…”

Section: Introductionmentioning

confidence: 98%

Emodin Retarded Renal Fibrosis Through Regulating HGF and TGFβ–Smad Signaling Pathway

Yang

Deng

et al. 2020

DDDT

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Background: Renal fibrosis is a frequently occurring type of chronic kidney disease that can cause end-stage renal disease. It has been verified that emodin or HGF can inhibit the development of renal fibrosis. However, the antifibrotic effect of emodin in combination with HGF remains unclear. Methods: Cell viability was detected with CCK8. Gene and protein expression in HK2 cells was detected by qRT-PCR and Western blot, respectively. Moreover, a unilateral ureteral obstruction-induced mouse model of renal fibrosis was established for investigating the antifibrotic effect of emodin in combination with HGF in vivo. Results: HGF notably increased the expression of collagen II in TGFβ-treated HK2 cells. In addition, HGF-induced increase in collagen II expression was further enhanced by emodin. In contrast, fibronectin, αSMA and Smad2 expression in TGFβ-stimulated HK2 cells was significantly inhibited by HGF and further decreased by combination treatment (emodin plus HGF). Moreover, we found that combination treatment exhibited better antifibrotic effects compared with emodin or HGF in vivo. Conclusion: These data demonstrated that emodin plus HGF exhibited better antifibrotic effects compared with emodin or HGF. As such, emodin in combination with HGF may serve as a new possibilty for treatment of renal fibrosis.

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Aloe-Emodin Ameliorates Renal Fibrosis Via Inhibiting PI3K/Akt/mTOR Signaling PathwayIn VivoandIn Vitro

Cited by 83 publications

References 46 publications

Cyclophosphamide Inhibits PI3K/AKT/mTOR Signaling Pathway in Mice Kidneys

Cyclophosphamide Inhibits PI3K/AKT/mTOR Signaling Pathway in Mice Kidneys

Exploring the Pharmacological Mechanism of Cassiae Semen a Cting on Cataracts Based on a Network Pharmacology Approach

<p>Emodin Retarded Renal Fibrosis Through Regulating HGF and TGFβ–Smad Signaling Pathway</p>

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