Regulatory Effect of 1,25(OH)2D3 on TGF-β1 and miR-130b Expression in Streptozotocin-Induced Diabetic Nephropathy in Rats

Liu, Yuetong; Yang, Ye; Wang, Qin; Kahaer, Apaer; Zhang, Jiyun; Liao, Jing; Abudureyimu, Mairemugu; Yahefu, Reyila; Qi, Jing; Zhao, Lei; Zhu, Jie

doi:10.1155/2019/1231346

Cited by 3 publications

(3 citation statements)

References 31 publications

(28 reference statements)

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“…Globally, there are 366 million DM patients and the numbers of new cases are predicted to double up by the year 2030. 1 Diabetic nephropathy (DN) is a common disorder that occurs because of both type 1 and type 2 DM and affects DM-associated mortality drastically. It is also responsible for renal dysfunction in high-income countries.…”

Section: Introductionmentioning

confidence: 99%

Apigenin-Loaded Solid Lipid Nanoparticle Attenuates Diabetic Nephropathy Induced by Streptozotocin Nicotinamide Through Nrf2/HO-1/NF-kB Signalling Pathway

Li¹,

Bukhari²,

Khan³

et al. 2020

IJN

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Background: Apigenin is known to have a broad-spectrum efficacy in oxidative stress and conditions due to inflammation, although weak absorption, fast metabolic rate and a fast elimination (systemic) limit the pharmacological efficacy of this drug. Hence, we propose the usage of highly bioavailable Apigenin-solid lipid nanoparticles (SLNPs) to recognize such limitations. The defensive function of Apigenin-SLNPs on renal damage induced by streptozotocin (STZ) in animals was studied. Materials and Methods: We initially injected the rats with 35 mg kg −1 streptozocin intraperitoneally, and after 7 days, the rats were then injected 150 mg kg −1 of metformin intragastrically followed by a once-daily intragastric dose of Apigenin-SLNP (25 or 50 mg kg −1) for a continuous period of 30 days. We then measured the level of insulin and blood glucose, superoxide dismutase, catalase and malondialdehyde in the tissues of the kidney. We also observed messenger-RNA expression of Interleukin-1β, Interleukin-6 and Tumor Necrosis Factor-alpha in renal tissue through RT-PCR technique. Moreover, H&E staining and Western blotting observed the histopathological variations and protein expression of nuclear factor erythroid 2-related factor 2/heme oxygenase/Nuclear Factor-κB signaling pathway, respectively. Results: An enhancement in the expressing of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 and a suppression in the expression of Nuclear Factor-κB occurred due to Apigenin-SLNPs treatment, which was a result of the protective mechanism of Apigenin-SLNPs which is because of not only its anti-inflammatory function (by inhibition of release of inflammatory factors) but also their anti-oxidant activity (through reduction of lipid peroxidation production). Conclusion: We found that a protective effect on diabetic nephropathy was shown due to Apigenin-SLNPs, in rats induced with streptozocin maybe through the pathway of nuclear factor erythroid 2-related factor 2/heme oxygenase-1/Nuclear Factor-κB.

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Section: Introductionmentioning

confidence: 99%

Apigenin-Loaded Solid Lipid Nanoparticle Attenuates Diabetic Nephropathy Induced by Streptozotocin Nicotinamide Through Nrf2/HO-1/NF-kB Signalling Pathway

Li¹,

Bukhari²,

Khan³

et al. 2020

IJN

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“…A previous study found that miR-130b reduced fat deposition in C57BL/6 mice, reversed glucose tolerance and improved high-fat diet-induced obesity ( 35 ). In addition, miR-130b has been shown to attenuate kidney fibrosis and damage induced by diabetes ( 36 ). The results of the present study indicated that the expression level of miR-130b was reduced in PC12 and hippocampal cells stimulated with high glucose.…”

Section: Discussionmentioning

confidence: 99%

miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy

Lei

Yang

et al. 2021

Int J Mol Med

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Diabetic encephalopathy (DE) is one of the main chronic complications of diabetes, and is characterized by cognitive defects. MicroRNAs (miRNAs/miRs) are widely involved in the development of diabetes-related complications. The present study evaluated the role of miR-130b in DE and investigated its mechanisms of action. PC12 cells and hippocampal cells were exposed to a high glucose environment to induce cell injuries to mimic the in vitro model of DE. Cells were transfected with miR-130b mimic, miR-130b inhibitor and small interfering RNA (si)-phosphatase and tensin homolog (PTEN) to evaluate the protective effect of the miR-130b/PTEN axis against oxidative stress in high glucose-stimulated cells involving Akt activity. Furthermore, the effect of agomir-130b was also assessed on rats with DE. The expression of miR-130b was reduced in the DE models in vivo and in vitro . The administration of miR-130b mimic increased the viability of high glucose-stimulated cells, prevented apoptosis, increased the activity of superoxide dismutase (SOD), decreased the malondialdehyde (MDA) content, activated Akt protein levels and inhibited the mitochondria-mediated apoptotic pathway. The administration of miR-130b inhibitor exerted opposite effects, while si-PTEN reversed the effects of miR-130b inhibitor. In vivo , the administration of agomir-130b attenuated cognitive disorders and neuronal damage, increased SOD activity, reduced the MDA content, activated Akt protein levels and inhibited the mitochondria-mediated apoptosis pathway in rats with DE. On the whole, these results suggest that miR-130b activates the PI3K/Akt signaling pathway to exert protective effects against oxidative stress injury via the regulation of PTEN in rats with DE.

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“…miR-21 not only suppresses the inhibitory Smad7 of TGF-β signaling to promote fibrosis (Zhong et al, 2013;Wang et al, 2014) but also targeting the Sprouty (SPRY) to activate the Ras/MEK/ERK signaling to activate fibrogenesis of TGF-β signaling (Xu et al, 2014). In addition, miR-21 also exerts profibrotic and pro-inflammatory Anti/pro-fibrosis (Kato et al, 2007;Chung et al, 2010;Krupa et al, 2010;Kato et al, 2011b;Putta et al, 2012;Deshpande et al, 2013;Ma et al, 2016;Liu et al, 2018) (Zhong et al, 2011;Wang et al, 2013;Zhong et al, 2013;Wang et al, 2014;Lai et al, 2015;Mcclelland et al, 2015;Kölling et al, 2017;Chen et al, 2018) Pro-inflammation miR-27a SFRP1; PRKAA2; PPARγ Pro-fibrosis (Hou et al, 2016;Wu et al, 2018b;Shi et al, 2020) miR-130b TGF-β1; Smad2/3; Smad4 (Castro et al, 2014;Lv et al, 2015;Liu et al, 2019b;Ma et al, 2019b) effects by targeting PTEN, tissue inhibitor of matrix metalloproteinases (TIMPs), and other molecules, as shown in Table 3.…”

Section: Tgf-β/smad-dependent Mirnas In Renal Fibrosis and Inflammation In Dkdmentioning

confidence: 99%

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

Huang

et al. 2021

Front. Pharmacol.

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Diabetic kidney disease (DKD) is the most common diabetic complication and is a leading cause of end-stage kidney disease. Increasing evidence shows that DKD is regulated not only by many classical signaling pathways but also by epigenetic mechanisms involving chromatin histone modifications, DNA methylation, and non-coding RNA (ncRNAs). In this review, we focus on our current understanding of the role and mechanisms of ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in the pathogenesis of DKD. Of them, the regulatory role of TGF-β/Smad3-dependent miRNAs and lncRNAs in DKD is highlighted. Importantly, miRNAs and lncRNAs as biomarkers and therapeutic targets for DKD are also described, and the perspective of ncRNAs as a novel therapeutic approach for combating diabetic nephropathy is also discussed.

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Regulatory Effect of 1,25(OH)2D3 on TGF-β1 and miR-130b Expression in Streptozotocin-Induced Diabetic Nephropathy in Rats

Cited by 3 publications

References 31 publications

<p>Apigenin-Loaded Solid Lipid Nanoparticle Attenuates Diabetic Nephropathy Induced by Streptozotocin Nicotinamide Through Nrf2/HO-1/NF-kB Signalling Pathway</p>

<p>Apigenin-Loaded Solid Lipid Nanoparticle Attenuates Diabetic Nephropathy Induced by Streptozotocin Nicotinamide Through Nrf2/HO-1/NF-kB Signalling Pathway</p>

miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

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