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Source: J Cell Mol Med
Condition: Diabetes

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Total 22 results found since Jan 2013.

A ketogenic diet improves vascular hyperpermeability in type 2 diabetic mice by downregulating vascular pescadillo1 expression
This study probes the role of PES1 and its mediated molecular mechanism in modulating vascular hyperpermeability in diabetic mice. Male C57BL/6J and db/db mice were fed a standard diet and a ketogenic diet (KD). Meanwhile, mouse vascular endothelial cells (MVECs) were treated with β-hydroxybutyric acid (β-HB), Pes1 siRNA or a Pes1 overexpression plasmid. Additionally, knockout (KO) of Pes1 in mice was applied. After 12 weeks of feedings, enhanced vascular PES1 expression in diabetic mice was inhibited by the KD. The suppression of PES1 was also observed in β-HB-treated MVECs. In mice with Pes1 KO, the levels of vascular...
Source: J Cell Mol Med - April 15, 2023 Category: Molecular Biology Authors: Song Wang Jielin Zhou Jing Lu Yan Lin Shuaishuai Liu Keyang Chen Source Type: research

Dapagliflozin alleviates cardiac fibrosis through suppressing EndMT and fibroblast activation via AMPK α/TGF-β/Smad signalling in type 2 diabetic rats
This study aimed to evaluate the effect of SGLT2 inhibitor dapagliflozin (DAPA) on DCM especially for cardiac fibrosis and explore the underlying mechanism. In vivo, the model of type 2 diabetic rats was built with high-fat feeding and streptozotocin injection. Untreated diabetic rats showed cardiac dysfunction, increased myocardial fibrosis and EndMT, which was attenuated after treatment with DAPA and metformin. In vitro, HUVECs and primary cardiac fibroblasts were treated with DAPA and exposed to high glucose (HG). HG-induced EndMT in HUVECs and collagen secretion of fibroblasts were markedly inhibited by DAPA. Up-regula...
Source: J Cell Mol Med - June 25, 2021 Category: Molecular Biology Authors: Jingjing Tian Mingjun Zhang Mengying Suo Dian Liu Xuyang Wang Ming Liu Jinyu Pan Tao Jin Fengshuang An Source Type: research

AMPK inhibits Smad3-mediated autoinduction of TGF- β1 in gastric cancer cells.
AMPK inhibits Smad3-mediated autoinduction of TGF-β1 in gastric cancer cells. J Cell Mol Med. 2021 Feb 03;: Authors: Zou J, Li C, Jiang S, Luo L, Yan X, Huang D, Luo Z Abstract We have previously shown that adenine monophosphate-activated protein kinase (AMPK) regulates transforming growth factor β (TGF-β)-triggered Smad3 phosphorylation. Here we report that AMPK inhibits TGF-β1 production. First, metformin reduced mRNA levels of TGF-β1 in gastric cancer cells, in parallel to the decrease of its protein abundance. The effects were more prominent in the cells containing LKB1, an upstream kinase of...
Source: J Cell Mol Med - February 3, 2021 Category: Molecular Biology Authors: Zou J, Li C, Jiang S, Luo L, Yan X, Huang D, Luo Z Tags: J Cell Mol Med Source Type: research

Loureirin B activates GLP-1R and promotes insulin secretion in Ins-1 cells.
Abstract Loureirin B (LB) is a natural product derived from Sanguis draconis, which has hypoglycaemic effects. In order to research the possible target of LB in the treatment of diabetes, molecular docking was used to simulate the interaction between LB and potential targets, and among them, glucagon-like peptide-1 receptor (GLP-1R) had the optimal results. Further, spectroscopy and surface plasmon resonance (SPR) experiments were applied to detect the interaction between LB and GLP-1R. Ultimately, after GLP-1R siRNA interfering the expression of GLP-1R in Ins-1 cell, the promoting insulin secretion of LB was weak...
Source: J Cell Mol Med - December 10, 2020 Category: Molecular Biology Authors: Ding Y, Xia S, Zhang H, Chen Q, Niu B Tags: J Cell Mol Med Source Type: research

Loss of lncRNA MIAT ameliorates proliferation and fibrosis of diabetic nephropathy through reducing E2F3 expression.
In this study, we tested expression level of MIAT in DN patients and mesangial cells treated by high glucose (HG). Up-regulation of MIAT was observed in DN. Then, functional assays displayed that silence of MIAT by siRNA significantly repressed the proliferation and cycle progression in mesangial cells induced by HG. Meanwhile, we found that collagen IV, fibronectin and TGF-β1 protein expression was obviously triggered by HG, which could be rescued by loss of MIAT. Then, further assessment indicated that MIAT served as sponge harbouring miR-147a. Moreover, miR-147a was decreased in DN, which exhibited an antagonistic effe...
Source: J Cell Mol Med - October 2, 2020 Category: Molecular Biology Authors: Ji TT, Qi YH, Li XY, Tang B, Wang YK, Zheng PX, Li W, Qu X, Feng L, Bai SJ Tags: J Cell Mol Med Source Type: research

HDAC6-mediated α-tubulin deacetylation suppresses autophagy and enhances motility of podocytes in diabetic nephropathy.
Abstract Histone deacetylase 6 (HDAC6) is the specific subtype of HDACs which preferentially located in the cytoplasm, and is crucial in insulin signalling. However, the role of HDAC6 in type 2 diabetic nephropathy (DN) remains undefined. In current study, we observed that HDAC6 was markedly activated in the kidneys of type 2 diabetic patients and db/db mice with albuminuria, along with the advanced glycation end products (AGE)-treated podocytes. Selective inhibition of HDAC6 activity protected kidneys from hyperglycaemia in db/db mice. Notably, overexpressing HDAC6 inhibited autophagy and promoted motility aside ...
Source: J Cell Mol Med - September 3, 2020 Category: Molecular Biology Authors: Liang T, Qi C, Lai Y, Xie J, Wang H, Zhang L, Lin T, Jv M, Li J, Wang Y, Zhang Y, Chen Z, Qiu X, Li R, Li Z, Ye Z, Liu S, Liang X, Shi W, Wang W Tags: J Cell Mol Med Source Type: research

Tacrolimus ameliorates tubulointerstitial inflammation in diabetic nephropathy via inhibiting the NFATc1/TRPC6 pathway.
Abstract Tubulointerstitial inflammation is crucial for the progression of diabetic nephropathy (DN), and tubular cells act as a driving force in the inflammatory cascade. Emerging data suggested that tacrolimus (TAC) ameliorates podocyte injury and macrophage infiltration in streptozotocin (STZ) mice. However, the effect of TAC on tubulointerstitial inflammation remains unknown. We found that albuminuria and tubulointerstitial damage improved in db/db mice treated with TAC. Macrophage infiltration and expression of IL-6, TNF-α, fibronectin, collagen 1 and cleaved caspase 3 were inhibited as well. In addition, th...
Source: J Cell Mol Med - August 10, 2020 Category: Molecular Biology Authors: Zhang S, Wang H, Liu Y, Yang W, Liu J, Han Y, Liu Y, Liu F, Sun L, Xiao L Tags: J Cell Mol Med Source Type: research

Diabetes aggravates myocardial ischaemia reperfusion injury via activating Nox2-related programmed cell death in an AMPK-dependent manner.
This study was designed to expose the crosstalk between oxidative stress and AMPK, a vital molecule that controls biological energy metabolism, in myocardial ischaemia reperfusion injury (I/RI) in diabetic rats. Diabetes was stimulated in rats using streptozotocin injection. Rats were separated on random into control, control + I/R, Diabetes, Diabetes + I/R, Diabetes + I/R + N-acetylcysteine and Diabetes + I/R + Vas2870 groups. Myocardial infarct size was determined, and the predominant Nox family isoforms were analysed. In vitro, the H9C2 cells were administered excess glucose and exposed to hypoxia/reoxygenat...
Source: J Cell Mol Med - April 28, 2020 Category: Molecular Biology Authors: Wang C, Zhu L, Yuan W, Sun L, Xia Z, Zhang Z, Yao W Tags: J Cell Mol Med Source Type: research

Knockout of AKAP150 improves impaired BK channel-mediated vascular dysfunction through the Akt/GSK3 β signalling pathway in diabetes mellitus.
In this study, we investigated the regulation of impaired BK channel-mediated vascular dysfunction in diabetes mellitus. Using AKAP150 null mice (AKAP150-/- ) and wild-type (WT) control mice (C57BL/6J), diabetes was induced by intraperitoneal injection of streptozotocin. We found that knockout of AKAP150 reversed vascular remodelling and fibrosis in mice with diabetes and in AKAP150-/- diabetic mice. Impaired Akt/GSK3β signalling contributed to decreased BK-β1 expression in aortas from diabetic mice, and the silencing of AKAP150 increased Akt phosphorylation and BK-β1 expression in MOVAS cells treated with HG medium. Th...
Source: J Cell Mol Med - March 11, 2020 Category: Molecular Biology Authors: Zhu YR, Jiang XX, Ye P, Wang ZM, Zheng Y, Liu Z, Chen SL, Zhang DM Tags: J Cell Mol Med Source Type: research

Inhibition of PHLPP1 ameliorates cardiac dysfunction via activation of the PI3K/Akt/mTOR signalling pathway in diabetic cardiomyopathy.
CONCLUSION: Our study indicated that PHLPP1 inhibition alleviated cardiac dysfunction via activating the PI3K/Akt/mTOR signalling pathway in DCM. Therefore, PHLPP1 may be a novel therapeutic target for human DCM. PMID: 32150791 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - March 8, 2020 Category: Molecular Biology Authors: Zhang M, Wang X, Liu M, Liu D, Pan J, Tian J, Jin T, Xu Y, An F Tags: J Cell Mol Med Source Type: research

Allopurinol reduces oxidative stress and activates Nrf2/p62 to attenuate diabetic cardiomyopathy in rats.
Abstract Allopurinol (ALP) attenuates oxidative stress and diabetic cardiomyopathy (DCM), but the mechanism is unclear. Activation of nuclear factor erythroid 2-related factor 2 (Nrf2) following the disassociation with its repressor Keap1 under oxidative stress can maintain inner redox homeostasis and attenuate DCM with concomitant attenuation of autophagy. We postulated that ALP treatment may activate Nrf2 to mitigate autophagy over-activation and consequently attenuate DCM. Streptozotocin-induced type 1 diabetic rats were untreated or treated with ALP (100 mg/kg/d) for 4 weeks and terminated after heart functi...
Source: J Cell Mol Med - December 18, 2019 Category: Molecular Biology Authors: Luo J, Yan D, Li S, Liu S, Zeng F, Cheung CW, Liu H, Irwin MG, Huang H, Xia Z Tags: J Cell Mol Med Source Type: research

Inhibition of P53/miR-34a improves diabetic endothelial dysfunction via activation of SIRT1.
Abstract Endothelial dysfunction contributes to diabetic macrovascular complications, resulting in high mortality. Recent findings demonstrate a pathogenic role of P53 in endothelial dysfunction, encouraging the investigation of the effect of P53 inhibition on diabetic endothelial dysfunction. Thus, high glucose (HG)-treated endothelial cells (ECs) were subjected to pifithrin-α (PFT-α)-a specific inhibitor of P53, or P53-small interfering RNA (siRNA), both of which attenuated the HG-induced endothelial inflammation and oxidative stress. Moreover, inhibition of P53 by PFT-α or P53-siRNA prohibited P53 acetylatio...
Source: J Cell Mol Med - February 22, 2019 Category: Molecular Biology Authors: Wu J, Liang W, Tian Y, Ma F, Huang W, Jia Y, Jiang Z, Wu H Tags: J Cell Mol Med Source Type: research

Endoplasmic reticulum stress-dependent autophagy inhibits glycated high-density lipoprotein-induced macrophage apoptosis by inhibiting CHOP pathway.
This study was designed to explore the inductive effect of glycated high-density lipoprotein (gly-HDL) on endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP)-mediated macrophage apoptosis and its relationship with autophagy. Our results showed that gly-HDL caused macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2α, and CHOP up-regulation, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and th...
Source: J Cell Mol Med - February 12, 2019 Category: Molecular Biology Authors: Tian H, Li Y, Kang P, Wang Z, Yue F, Jiao P, Yang N, Qin S, Yao S Tags: J Cell Mol Med Source Type: research