Paeoniflorin ameliorates Adriamycin-induced nephrotic syndrome through the PPARγ/ANGPTL4 pathway in vivo and vitro

Lu, Ruirui; Zhou, Jie; Liu, Bihao; Ning, Liang; He, Yu; Bai, Lin; Zhong, Yanqiang; Zhou, Yuan; Zhou, Jiuyao

doi:10.1016/j.biopha.2017.09.105

Cited by 37 publications

(24 citation statements)

References 43 publications

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“…Paeoniflorin exhibits numerous pharmacological effects, such as anti-inflammation, immunomodulation, antioxidation and anti-proliferation of cancer cells (Gu et al, 2016; Zhai et al, 2016; Song et al, 2017; Zhang et al, 2018). Recent research and our previous study found that paeoniflorin improved some experimental models of kidney disease, including diabetic nephropathy (Zhang et al, 2017), nephrotic syndrome (Lu et al, 2017), acute renal injury (Wang et al, 2016) and renal fibrosis (Zeng et al, 2013). More importantly, paeoniflorin ameliorated advanced glycation end product (AGE)-induced mesangial cell injury partly by anti-inflammation (Zhang et al, 2013; Chen et al, 2017).…”

Section: Introductionmentioning

confidence: 95%

Paeoniflorin Inhibits Mesangial Cell Proliferation and Inflammatory Response in Rats With Mesangial Proliferative Glomerulonephritis Through PI3K/AKT/GSK-3β Pathway

et al. 2019

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Mesangial proliferative glomerulonephritis (MPGN) is the most common type of chronic kidney disease in China, characterized by mesangial cell proliferation and inflammatory response. Paeoniflorin, an effective composition extracted from Radix Paeoniae Alba, has been used for various kinds of kidney diseases. However, there are no studies reporting the effects of paeoniflorin on MPGN. The present study aims to investigate whether paeoniflorin plays a role in MPGN and confirm the underlying molecular mechanisms. Our results manifested that paeoniflorin strongly restrained 24 h urinary protein and promoted renal function and dyslipidemia in a MPGN rat model. Moreover, paeoniflorin attenuated mesangial cell proliferation and inflammation both in MPGN rats and human mesangial cells (HMCs) treated with lipopolysaccharide (LPS). In detail, paeoniflorin decreased the number of mesangial cells and expressions of proliferation marker Ki67 in MPGN rats. Paeoniflorin also inhibited HMC proliferation and blocked cell cycle progression. In addition, the contents of inflammatory factors and the expressions of macrophage marker iNOS were decreased after paeoniflorin treatment. Furthermore, we found that the protective effect of paeoniflorin was accompanied by a strong inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT/glycogen synthase kinase (GSK)-3β pathway. Paeoniflorin enhanced the inhibitory effect of PI3K inhibitor LY294002 and suppressed the activated effect of PI3K agonist insulin-like growth factor 1 (IGF-1) on PI3K/AKT/GSK-3β pathway. In conclusion, these results demonstrated that paeoniflorin ameliorates MPGN by inhibiting mesangial cell proliferation and inflammatory response through the PI3K/AKT/GSK-3β pathway.

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Section: Introductionmentioning

confidence: 95%

Paeoniflorin Inhibits Mesangial Cell Proliferation and Inflammatory Response in Rats With Mesangial Proliferative Glomerulonephritis Through PI3K/AKT/GSK-3β Pathway

et al. 2019

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“…Using genome-wide transcriptional profiling technology, Kaddatz et al [ 38 ] reported that human ANGPTL4 expression might be synergistically induced by the functional interactions of transforming growth factor-β (TGF-β) and PPARβ/δ signaling. Agonists such as PPAR agonists, protein kinase C (PKC) agonists, retinoic acid receptors (RXR) agonists, HIF-1α agonists, glucocorticoid receptor agonists, and angiotensin receptor blockers, drugs such as paeoniflorin, glucocorticoids, chiglitazar, fibrates, thiazolidinediones, PMA, 1,2-dioctanoyl-sn-glycerol (DOG), bryostatin, L-mimosine (L-MIM), advanced glycation end products (AGEs) and dexamethasone [ 32 , 39–43 ], inhibitors of known receptors (such as angiotensin blockers, resistin, leptin, and insulin [ 44 ]), and inflammation molecules (such as lipase, tumor necrosis factor-α, interleukin-1β, and interferon-γ [ 45 , 46 ]) were shown to regulate the expression of ANGPTL4. HIF-1α induction of ANGPTL4 under hypoxic conditions was first described in cardiomyocytes but also occurs in other cell types including adipocytes, endothelial cells, chondrocytes, monocytes, musculoskeletal cells, osteoclasts, and osteoblasts [ 47 ].…”

Section: Angptl4: Structure and Expression Patternsmentioning

confidence: 99%

A review of the multifunctionality of angiopoietin-like 4 in eye disease

Yang

Cheng

2018

Bioscience Reports

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Angiopoietin-like protein 4 (ANGPTL4) is a multifunctional cytokine regulating vascular permeability, angiogenesis, and inflammation. Dysregulations in these responses contribute to the pathogenesis of ischemic retinopathies such as diabetic retinopathy (DR), age-related macular degeneration (AMD), retinal vein occlusion, and sickle cell retinopathy (SCR). However, the role of ANGPTL4 in these diseases remains controversial. Here, we summarize the functional mechanisms of ANGPTL4 in several diseases. We highlight original studies that provide detailed data about the mechanisms of action for ANGPTL4, its applications as a diagnostic or prognostic biomarker, and its use as a potential therapeutic target. Taken together, the discussions in this review will help us gain a better understanding of the molecular mechanisms by which ANGPTL4 functions in eye disease and will provide directions for future research.

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“…ANGPTL4 could elevate O 2 -produc- [21]. Moreover, inhibiting ANGPTL4 could also decrease cell apoptosis and meliorate the Adriamycin-induced nephrotic syndrome [42]. In our study, when treated with Adriamycin, the ANGPTL4 expression significantly upregulated, suggesting that ANGPTL4 may be involved in FSGS.…”

Section: Discussionmentioning

confidence: 49%

Epigallocatechin-3-Gallate Attenuates Adriamycin-Induced Focal Segmental Glomerulosclerosis via Suppression of Oxidant Stress and Apoptosis by Targeting Hypoxia-Inducible Factor-1α/ Angiopoietin-Like 4 Pathway

Liu¹,

2019

Pharmacology

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Background: Focal and segmental glomerular sclerosis (FSGS) is a common cause of nephrotic syndrome and end-stage renal disease. It has been reported that overproduction of reactive oxygen species (ROS) and cell apoptosis are associated with the development of FSGS. Epigallocatechin-3-gallate (EGCG) is a bioactive constituent accounting for more than 50% of the total catechins in green tea, which have anti-oxidative and anti-apoptotic effects. Based on this, this study was designed to evaluate the renoprotective effect of EGCG treatment on Adriamycin-induced FSGS. Methods: In C57BL/6 mice, Adriamycin nephropathy (AN) was induced by Adriamycin (10 mg/kg body weight, diluted in normal saline) via a tail vein on day 0. Then the mice were given with EGCG (20 mg/kg body weight) or YC-1 (Lificiguat, a specific inhibitor of hypoxia-inducible factor-1α [HIF-1α], 50 mg/kg body weight) or both intraperitoneally. Both the EGCG and YC-1 were given on the day of Adriamycin injection and continued for 6 weeks. The animals were organized into the following 5 groups for the animal experiments: the control group, the AN group, the AN + EGCG group, the AN + YC-1 group and the AN + EGCG + YC-1 group. At 6 weeks, the mice were sacrificed; kidneys and blood samples were collected for further analysis. The HIF-1α and the angiopoietin-like 4 (ANGPTL4) expression were detected by Western blot, real-time PCR, immunohistochemistry or immunofluorescence. Dihydroethidium staining and NADPH oxidase 1 (Nox1) measurement were used to detect ROS production. Terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL) staining and caspase-3 measurement was used to detect cell apoptosis. Results: When the animals were treated with Adriamycin, both the ROS production and TUNEL positive cells increased. Besides, the expression of HIF-1α, ANGPTL4, and caspase-3 were also up-regulated, while EGCG treatment could attenuate these changes. Interestingly, compared with treatment with YC-1 or EGCG alone, more pronounced inhibition of ANGPTL4, caspase-3 and Nox1 were obtained when YC-1 and EGCG were administered simultaneously. Conclusion: EGCG attenuates FSGS through the suppression of Oxidant Stress and apoptosis by targeting the HIF-1α/ANGPTL4 pathway.

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Paeoniflorin ameliorates Adriamycin-induced nephrotic syndrome through the PPARγ/ANGPTL4 pathway in vivo and vitro

Cited by 37 publications

References 43 publications

Paeoniflorin Inhibits Mesangial Cell Proliferation and Inflammatory Response in Rats With Mesangial Proliferative Glomerulonephritis Through PI3K/AKT/GSK-3β Pathway

Paeoniflorin Inhibits Mesangial Cell Proliferation and Inflammatory Response in Rats With Mesangial Proliferative Glomerulonephritis Through PI3K/AKT/GSK-3β Pathway

A review of the multifunctionality of angiopoietin-like 4 in eye disease

Epigallocatechin-3-Gallate Attenuates Adriamycin-Induced Focal Segmental Glomerulosclerosis via Suppression of Oxidant Stress and Apoptosis by Targeting Hypoxia-Inducible Factor-1α/ Angiopoietin-Like 4 Pathway

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