Retracted Article: Ligustrazine attenuates renal damage by inhibiting endoplasmic reticulum stress in diabetic nephropathy by inactivating MAPK pathways

Yang, Haitao; Wu, Shuizhu

doi:10.1039/c8ra01674g

Cited by 11 publications

(8 citation statements)

References 36 publications

(39 reference statements)

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“…Our findings are just consistent with previous studies, and illustrate that the inflammatory response is relieved by the up-regulation of miR-451 in H-GMCs. In addition, it has been proved that some agents exhibit great potential in the treatment of DN via inhibiting pro-inflammatory cytokines, such as resveratrol [28], ligustrazine [29], notoginsenoside R1 [30], and ellagic acid [15]. We suspect that the up-regulation of miR-451 may protect against DN through relieving inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-451 inhibits inflammation and proliferation of glomerular mesangial cells through down-regulating PSMD11 and NF-κB p65

Hua

et al. 2019

Bioscience Reports

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The present study aimed to investigate the regulatory roles of microRNA-451 (miR-451) on the inflammation and proliferation of glomerular mesangial cells (GMCs) under high-glucose condition, and reveal the potential mechanisms related to 26S proteasome non-ATPase regulatory subunit 11 (PSMD11) and nuclear factor-κ B (NF-κB) signaling. The interaction between PSMD11 and miR-451 was identified by dual luciferase reporter (DLR) gene assay. GMCs were treated with 5.6 mmol/l (normal, L-GMCs) and 30 mmol/l glucose (high-glucose, H-GMCs), respectively. After transfecting with pcDNA3.1-PSMD11 and/or miR-451 mimics, the expression of miR-451, PSMD11, inhibitor of NF-κB α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65, COX-2, and cyclinD1 were detected in H-GMCs by quantitative real-time PCR (qRT-PCR) and/or Western blot. The levels of interleukin (IL)-1β, IL-6, and IL-8, cell cycle, and viability was detected by enzyme-linked immunosorbent assay, flow cytometry, and MTT assay, respectively. MiR-451 was up-regulated in H-GMCs, and negatively regulated its target PSMD11 (P<0.05). H-GMCs exhibited significantly higher levels of IL-1β, IL-6, and IL-8, cell viability, and p-IκBα, NF-κB, COX-2, and cyclinD1 expression than L-GMCs (P<0.05). The transfection of miR-451 mimics significantly decreased the levels of IL-1β, IL-6, and IL-8, inhibited the cell viability via blocking cells in G0/G1 phase, and down-regulated p-IκBα, NF-κB p65, COX-2, and cyclinD1 in H-GMCs (P<0.05). The regulatory effects of miR-451 mimics on H-GMCs were reversed by the transfection of PSMD11 (P<0.05). The up-regulation of miR-451 inhibits the inflammation and proliferation of H-GMCs through down-regulating PSMD11 and NF-κB p65.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-451 inhibits inflammation and proliferation of glomerular mesangial cells through down-regulating PSMD11 and NF-κB p65

Hua

et al. 2019

Bioscience Reports

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“…The PI3k/Akt/mTOR signaling pathway is currently known as the only inhibitory pathway for autophagy, and its activation can inhibit autophagy. Zhong et al [ 35 ] found that ligustrazine can inhibit the expression of p-PI3K, p-Akt, and p-mTOR in the kidney tissues of diabetic rats, thereby, increasing the expression level of the autophagy marker protein LC3B and the ratio of LC3B-II/LC3B-I. The results of this experiment indicate that the PI3k/Akt/mTOR signaling pathway is activated, and autophagy is inhibited in diabetic nephropathy; however, the signaling pathway is inhibited, and autophagy is reactivated after GLP treatment, indicating that GLP plays a renal protective role.…”

Section: Discussionmentioning

confidence: 99%

Effects and Mechanism of Ganoderma lucidum Polysaccharides in the Treatment of Diabetic Nephropathy in Streptozotocin-Induced Diabetic Rats

Wang

et al. 2022

BioMed Research International

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Ganoderma lucidum polysaccharides (GLP) have renal protection effect but there was no study on the diabetic nephropathy. This study was designed to investigate its effect and mechanism using a diabetic rat model induced by streptozotocin (50 mg/kg, i.p.). The diabetic rats were treated with GLP (300 mg/kg/day) for 10 weeks. The blood glucose, glycated hemoglobin, body weight, and the levels of blood creatinine, urea nitrogen, and urine protein were assessed. And renal pathologies were assessed by the tissue sections stained with hematoxylin-eosin, Masson’s trichome, and periodic acid-Schiff. The expression of phosphorylated phosphoinositide 3 kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), and phosphorylated mammalian target of rapamycin (p-mTOR), the autophagy proteins beclin-1, LC3-II, LC3-I, and P62; the apoptosis-related proteins caspase-3 and caspase-9; and the inflammation markers IL-6, IL-1β, and TNF-ɑ were assessed. Results showed that GLP alleviated the impairment of renal function by reducing urinary protein excretion and the blood creatinine level and ameliorated diabetic nephropathy. The expression of p-PI3K, p-Akt, and p-mTOR in the diabetic kidney were significantly reduced in the GLP treatment group compared to the without treatment group. GLP treatment activated the autophagy indicators of beclin-1 and the ratio of LC3-II/LC3-I but reduced p62 and also inhibited the expression of caspase-3, caspase-9 and IL-6, IL-1β, and TNF-ɑ. In conclusion, the effect of GLP amelioration diabetic nephropathy may be via the PI3k/Akt/mTOR signaling pathway by inhibition of the apoptosis and inflammation and activation of the autophagy process.

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“…In the year 2018, several compounds like berberine, gallic acid, ligustrazine, nifuroxazide, pentoxifylline, rosuvastatin, and so forth to treat kidney damage in type 1 diabetes and compounds like dihydroquercetin, cinacalcet, cyanidin‐3‐O‐glucoside, zingerone, glucagon‐like peptide‐1 (GLP‐1) co‐agonist, dapagliflozin, pioglitazone, and fibroblast growth factor 1 to treat kidney damage in type 2 diabetes have been studied so far. Compound like carnosic acid was found to ameliorate kidney damage in both type 1 and type 2 diabetes (Ding et al, ; Elhawary, Ibrahim, & Attallah, ; Elsherbiny, Zaitone, Mohammad, & El‐Sherbiny, ; Garud & Kulkarni, ; Han et al, ; Liang et al, ; Lim et al, ; Patel et al, ; Qin et al, ; Rehman et al, ; Xie et al, ; Yang & Wu, ; Zhu, Han, Yuan, Xue, & Pang, ).…”

Section: Introductionmentioning

confidence: 99%

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Jash

Gondaliya

Kirave

et al. 2019

Drug Development Research

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Diabetes mellitus (DM) is a gradually rising metabolic disease which is currently affecting millions of people worldwide. Diabetes is associated with various complications like nephropathy, neuropathy, retinopathy, diabetic foot, cognitive impairment, and many more. Evidence suggests that cognitive dysfunction is a rising complication of diabetes which adversely affects the brain of patients suffering from diabetes. Age‐related memory impairment is a complication having its major effect on people suffering from diabetes and Alzheimer's. Patients suffering from diabetes are at two times higher risk of developing cognitive dysfunction as compared with normal individuals. Multiple factors which are involved in diabetes related complications are found to play a role in the development of neurodegeneration in Alzheimer's. The problem of insulin deficiency and insulin resistance is well reported in diabetes but there are many studies which suggest dysregulation of insulin levels as a reason behind the development of Alzheimer's. As the link between diabetes and Alzheimer disease (AD) is deepening, there is a need to understand the plausible tie‐ins between the two. Emerging role of major factors like insulin imbalance, advanced glycation end products and micro‐RNA's involved in diabetes and Alzheimer's have been discussed here. This review helps in understanding the plausible mechanism underlying the pathophysiology of amyloid beta (Aβ) plaque formation and tau hyperphosphorylation as well provides information about studies carried out in this area of research. The final thought is to enhance the scientific knowledge on this correlation and develop future therapeutics to treat the same.

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Retracted Article: Ligustrazine attenuates renal damage by inhibiting endoplasmic reticulum stress in diabetic nephropathy by inactivating MAPK pathways

Abstract: Diabetic nephropathy (DN) is a major cause of chronic kidney disease around the world.

Cited by 11 publications

References 36 publications

MicroRNA-451 inhibits inflammation and proliferation of glomerular mesangial cells through down-regulating PSMD11 and NF-κB p65

MicroRNA-451 inhibits inflammation and proliferation of glomerular mesangial cells through down-regulating PSMD11 and NF-κB p65

Effects and Mechanism of Ganoderma lucidum Polysaccharides in the Treatment of Diabetic Nephropathy in Streptozotocin-Induced Diabetic Rats

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

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