Protective effect of Citrullus colocynthis (L.) Schard. fruit extract on high glucose-induced neurotoxicity in PC-12 cells

Myrciaria dubia (HBK) McVaugh (camu-camu) belongs to the family Myrtaceae. Although camu-camu has received a great deal of attention for its potential pharmacological activities, there is little information on the anti-oxidative stress and anti-inflammatory effects of camu-camu fruit in skin diseases. In the present study, we investigated the preventative effect of 70% ethanol camu-camu fruit extract against high glucose-induced human keratinocytes. High glucose-induced overproduction of reactive oxygen species (ROS) was inhibited by camu-camu fruit treatment. In response to ROS reduction, camu-camu fruit modulated the mitogen-activated protein kinases (MAPK)/activator protein-1 (AP-1), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and nuclear factor of activated T cells (NFAT) signaling pathways related to inflammation by downregulating the expression of proinflammatory cytokines and chemokines. Furthermore, camu-camu fruit treatment activated the expression of nuclear factor E2-related factor 2 (Nrf2) and subsequently increased the NAD(P)H:quinone oxidoreductase1 (NQO1) expression to protect keratinocytes against high-glucose-induced oxidative stress. These results indicate that camu-camu fruit is a promising material for preventing oxidative stress and skin inflammation induced by high glucose level.

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Protective Effect of Heme Oxygenase-1 on High Glucose-Induced Pancreatic β-Cell Injury

Diabetes & Metabolism Journal ◽

10.4093/dmj.2011.35.5.469 ◽

2011 ◽

Vol 35 (5) ◽

pp. 469 ◽

Cited By ~ 14

Author(s):

Eun-Mi Lee ◽

Young-Eun Lee ◽

Esder Lee ◽

Gyeong Ryul Ryu ◽

Seung-Hyun Ko ◽

...

Keyword(s):

Protective Effect ◽

Heme Oxygenase ◽

High Glucose ◽

Cell Injury ◽

Heme Oxygenase 1 ◽

Pancreatic Β Cell ◽

Β Cell

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Protective Effect of Quercetin against H2O2-Induced Oxidative Damage in PC-12 Cells: Comprehensive Analysis of a lncRNA-Associated ceRNA Network

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/6038919 ◽

2020 ◽

Vol 2020 ◽

pp. 1-22

Author(s):

Zheyu Zhang ◽

Pengji Yi ◽

Min Yi ◽

Xiaoliang Tong ◽

Xin Cheng ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Oxidative Damage ◽

Protective Effect ◽

Messenger Rna ◽

Noncoding Rna ◽

Expression Profiles ◽

Damage Model ◽

Antioxidant Properties ◽

Pc 12 Cells ◽

Cerna Network

Quercetin is a bioflavonoid with potential antioxidant properties. However, the mechanisms underlying its effects remain unclear. Herein, we focused on integrating long noncoding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) sequencing of PC-12 cells treated with quercetin. We treated PC-12 cells with hydrogen peroxide to generate a validated oxidative damage model. We evaluated the effects of quercetin on PC-12 cells and established the lncRNA, miRNA, and mRNA profiles of these cells. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses of these RNAs were conducted to identify the key pathways. Quercetin significantly protected PC-12 neuronal cells from hydrogen peroxide-induced death. We identified 297, 194, and 14 significantly dysregulated lncRNAs, miRNAs, and mRNAs, respectively, associated with the antioxidant effect of quercetin. Furthermore, the phosphatidylinositol-3-kinase/protein kinase B pathway was identified as the crucial signalling pathway. Finally, we constructed a lncRNA-associated competing endogenous RNA (ceRNA) network by utilizing oxidative damage mechanism-matched miRNA, lncRNA, and mRNA expression profiles and those changed by quercetin. In conclusion, quercetin exerted a protective effect against oxidative stress-induced damage in PC-12 cells. Our study provides novel insight into ceRNA-mediated gene regulation in the progression of oxidative damage and the action mechanisms of quercetin.

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WITHDRAWN: Protective effect of Punica granatum fruit extract on inflammatory cytokines and antiangiogenic factors in endothelial cells induced by plasma from preeclamptic patients

Biomarkers and Genomic Medicine ◽

10.1016/j.bgm.2016.03.001 ◽

2016 ◽

Author(s):

Dewi Ambarwati ◽

Fatmawati Fatmawati ◽

Mukhamad Nooryanto ◽

Sanarto Santoso ◽

Siti Candra Windu Baktiyani ◽

...

Keyword(s):

Endothelial Cells ◽

Protective Effect ◽

Inflammatory Cytokines ◽

Punica Granatum ◽

Fruit Extract ◽

Antiangiogenic Factors

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Investigating the Protective Effect of Lithium Against High Glucose-Induced Neurotoxicity in PC12 Cells: Involvements of ROS, JNK and P38 MAPKs, and Apoptotic Mitochondria Pathway

Cellular and Molecular Neurobiology ◽

10.1007/s10571-014-0089-y ◽

2014 ◽

Vol 34 (8) ◽

pp. 1143-1150 ◽

Cited By ~ 27

Author(s):

A. Aminzadeh ◽

A. R. Dehpour ◽

M. Safa ◽

S. Mirzamohammadi ◽

A. M. Sharifi

Keyword(s):

Protective Effect ◽

Pc12 Cells ◽

High Glucose ◽

Mitochondria Pathway ◽

P38 Mapks

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Ethyl Rosmarinate Protects High Glucose-Induced Injury in Human Endothelial Cells

Molecules ◽

10.3390/molecules23123372 ◽

2018 ◽

Vol 23 (12) ◽

pp. 3372 ◽

Cited By ~ 3

Author(s):

Yan-Hui Shen ◽

Li-Ying Wang ◽

Bao-Bao Zhang ◽

Qi-Ming Hu ◽

Pu Wang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Endothelial Cells ◽

Protective Effect ◽

High Glucose ◽

Reactive Oxygen ◽

Annexin V ◽

Ros Generation ◽

Dependent Manner ◽

Oxygen Species ◽

Jnk Pathway

Ethyl rosmarinate (RAE) is one of the active constituents from Clinopodium chinense (Benth.) O. Kuntze, which is used for diabetic treatment in Chinese folk medicine. In this study, we investigated the protective effect of RAE on high glucose-induced injury in endothelial cells and explored its underlying mechanisms. Our results showed that both RAE and rosmarinic acid (RA) increased cell viability, decreased the production of reactive oxygen species (ROS), and attenuated high glucose-induced endothelial cells apoptosis in a dose-dependent manner, as evidenced by Hochest staining, Annexin V–FITC/PI double staining, and caspase-3 activity. RAE and RA both elevated Bcl-2 expression and reduced Bax expression, according to Western blot. We also found that LY294002 (phosphatidylinositol 3-kinase, or PI3K inhibitor) weakened the protective effect of RAE. In addition, PDTC (nuclear factor-κB, or NF-κB inhibitor) and SP600125 (c-Jun N-terminal kinase, or JNK inhibitor) could inhibit the apoptosis in endothelial cells caused by high glucose. Further, we demonstrated that RAE activated Akt, and the molecular docking analysis predicted that RAE showed more affinity with Akt than RA. Moreover, we found that RAE inhibited the activation of NF-κB and JNK. These results suggested that RAE protected endothelial cells from high glucose-induced apoptosis by alleviating reactive oxygen species (ROS) generation, and regulating the PI3K/Akt/Bcl-2 pathway, the NF-κB pathway, and the JNK pathway. In general, RAE showed greater potency than RA equivalent.

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Dapagliflozin Ameliorates Diabetic Kidney Disease via Upregulating Crry and Alleviating Complement Over-activation in db/db Mice

Frontiers in Pharmacology ◽

10.3389/fphar.2021.729334 ◽

2021 ◽

Vol 12 ◽

Author(s):

Dong-Yuan Chang ◽

Xiao-Qian Li ◽

Min Chen ◽

Ming-Hui Zhao

Keyword(s):

Kidney Disease ◽

Protective Effect ◽

High Glucose ◽

Diabetic Kidney Disease ◽

Membrane Attack Complex ◽

Sglt2 Inhibitors ◽

Tubulointerstitial Injury ◽

Diabetic Kidney ◽

Proximal Tubular Epithelial Cells ◽

Complement Regulator

Sodium-glucose cotransporter 2(SGLT2) inhibitors show prominent renal protective effect in diabetic kidney disease (DKD), anti-inflammatory effect being one of its key mechanisms. Over-activation of the complement system, a crucial part of innate immunity, plays an important role in DKD. We aimed to investigate the effect of SGLT2 inhibitors on alleviating complement over-activation in DKD. Db/db mice were randomly divided into two groups, with 7 mice in each group treated with dapagliflozin and vehicle respectively, and 7 mice in m/m mice group. Laboratory and renal pathological parameters were evaluated. Mouse proximal tubular epithelial cells (MPTECs) were cultured and treated with high glucose. Dapagliflozin and dimethyloxallyl glycine (DMOG) were added as conditional treatment. Dapagliflozin-treated db/db mice showed significantly lower urinary albumin than vehicle-treated ones. Besides typical glomerular and tubulointerstitial injury, both C3b and membrane attack complex (MAC) depositions were significantly attenuated in dapagliflozin-treated db/db mice. The expression of complement receptor type 1-related protein y (Crry), a key complement regulator which inhibits complement over-activation, was significantly upregulated by dapagliflozin. Dapagliflozin-mediated Crry upregulation was associated with inhibition of HIF-1α accumulation under high glucose. When HIF-1α expression was stabilized by DMOG, the protective effect of dapagliflozin via upregulating Crry was blocked. In conclusion, dapagliflozin could attenuate complement over-activation in diabetic mice via upregulating Crry, which is associated with the suppression of HIF-1α accumulation in MPTECs.

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