scholarly journals Protective Effects of Kaempferol on D-Ribose-Induced Mesangial Cell Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Ning Zhang ◽  
Shaoyang Zhao ◽  
Jinni Hong ◽  
Weiwei Li ◽  
Xuemei Wang
Keyword(s):  
Western Blot ◽  
Protective Effect ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Cell Damage ◽  
Membrane Integrity ◽  
Protective Effects ◽  
Ros Accumulation ◽  
Ldh Assay

Recently, it has been found that the level of urinary D-ribose in type 2 diabetes is notably higher than that in age-matched normal control, and D-ribose is more reactive in the glycation than D-glucose and induces oxidative stress. Kaempferol is one of the main bioactive components in Astragalus membranaceus, with numerous physiological actives, such as antioxidant. The present study investigated the protective effects of kaempferol on D-ribose-treated mesangial cells. CCK-8 and LDH assay were used to test cell viability and cell toxicity. Immunofluorescence and flow cytometry were used to detect the AGE formation and ROS accumulation. GSH level was measured to reflect oxidation resistance. Cell apoptosis was evaluated by Hoechst 33258 staining, AO/EB staining, and western blot. Mitochondrial membrane integrity was detected by JC-1 staining, western blot, and RT-PCR. The change of autophagy level was tested by western blot. The results indicated that D-ribose induced not only cell damage and increased AGE formation and ROS accumulation but also GSH depletion. Further studies demonstrated that D-ribose induced mitochondrial depolarization and the activation of caspase-9/3. But kaempferol could partly block these damages. Subsequently, it was confirmed that kaempferol repaired the autophagy disturbance induced by D-ribose, and 3-MA could reverse the protective effect of kaempferol under D-ribose condition. Our study demonstrated that D-ribose induced AGE accumulation and ROS production in mesangial cell and caused mitochondrial apoptosis, but kaempferol could attenuate these changes and its protective effect might be related to the repair of autophagy.

Mass spectrometry-based circulating IgA1 complexes screening driven identification of IgA-alpha-1-microglobulin complex in IgA nephropathy

2020 ◽  
Author(s):  
Boyang Xu ◽  
Li Zhu ◽  
Qingsong Wang ◽  
Yanfeng Zhao ◽  
Meng Jia ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Iga Nephropathy ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Independent Population ◽  
Tubulointerstitial Lesions ◽  
Noninvasive Biomarker

Abstract Background IgA nephropathy (IgAN) is characterized by predominant IgA deposition in the glomerular mesangium. Previous studies proved that renal-deposited IgA in IgAN came from circulating IgA1-containing complexes (CICs). Methods To explore the composition of CICs in IgAN, we isolated CICs from IgAN patients and healthy controls, and then quantitatively analyzed them by mass spectrometry. Meanwhile, the isolated CICs were used to treat human mesangial cells to monitor mesangial cell injury. Taken together the proteins content and injury effects, the key constituent in CICs was identified. Then, the circulating levels of identified key constituent-IgA complex were detected in an independent population by an in-house-developed ELISA. Results By comparing the proteins of CICs between IgAN patients and controls, we found that 14 proteins showed significantly different levels. Among them, alpha-1-microglobulin content in CICs was associated with not only in vitro mesangial cell proliferation and MCP-1 secretion but also in vivo eGFR levels and tubulointerstitial lesions in IgAN patients. Moreover, we found alpha-1-microglobulin was prone to bind aberrant glycosylated IgA1. Additionally, an elevated circulating IgA-alpha-1-microglobulin complex levels were detected in an independent IgAN population, and IgA-alpha-1-microglobulin complex levels were correlated with hypertension, eGFR levels and Oxford-T scores in these IgAN patients. Conclusions Our results suggest that the IgA-alpha-1-microglobulin complex is an important constituent in CICs, and that circulating IgA-alpha-1-microglobulin complex detection might serve as a potential noninvasive biomarker detection method for IgAN.

scholarly journals Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Jingxuan Sun ◽  
Boyu Yuan ◽  
Yancheng Wu ◽  
Yuhong Gong ◽  
Wenjin Guo ◽  
...  
Keyword(s):  
Sodium Butyrate ◽  
Cell Injury ◽  
Cell Damage ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Fatty Acid Salt ◽  
Cognitive Improvement ◽  
N2a Cells ◽  
Underlying Mechanisms

Alzheimer’s disease (AD) is a common neurodegenerative disease. Aβ plays an important role in the pathogenesis of AD. Sodium butyrate (NaB) is a short-chain fatty acid salt that exerts neuroprotective effects such as anti-inflammatory, antioxidant, antiapoptotic, and cognitive improvement in central nervous system diseases. The aim of this study is to research the protective effects of NaB on neurons against Aβ toxicity and to uncover the underlying mechanisms. The results showed that 2 mM NaB had a significant improvement effect on Aβ-induced N2a cell injury, by increasing cell viability and reducing ROS to reduce injury. In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF. Therefore, NaB protects N2a cells from Aβ-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.

scholarly journals Antioxidant Effects and Cytoprotective Potentials of Herbal Tea against H2O2-Induced Oxidative Damage by Activating Heme Oxygenase1 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ke-Xin Zhang ◽  
Jian-Bin Tan ◽  
Cheng-Liang Xie ◽  
Rong-Bo Zheng ◽  
Xiao-Dan Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Protective Effect ◽  
Functional Foods ◽  
Cell Damage ◽  
Damage Model ◽  
Enrichment Analysis ◽  
Protective Effects ◽  
Herbal Tea ◽  
Antioxidant Effects

Herbal tea with antioxidant ingredients has gained increasing attention in the field of functional foods due to their amelioration potential in aging-related diseases. Wanglaoji herbal tea (WHT) is a kind of traditional beverage made from herbal materials. This study was performed to investigate its antioxidant activity and identify its protective effect on a H2O2-induced cell damage model. In this study, we identified six kinds of phenolic acids with antioxidant activity in WHT, among which rosmarinic acid had the highest content and the highest contribution ratio to the antioxidant activity of WHT. Moreover, compared with the H2O2-induced damage group, the WHT treatment group can significantly increase the viability of cells and decrease the ratio of senescence-associated β-galactosidase-positive cells, intracellular malondialdehyde levels, and the percentage of G1 phase. Furthermore, enrichment analysis of differentially expressed genes revealed that heme oxygenase1 (HMOX1) was a key gene for protective effect of WHT on oxidative stress-induced cell damage. Thus, WHT exerted protective effects not only by scavenging reactive oxygen species but also by inducing the expression of cytoprotective genes by activating the HMOX1 pathway, which showed that WHT had a potential of promoting health by reducing oxidative stress-induced cell damage.

scholarly journals Perilla frutescens Sprout Extract Protect Renal Mesangial Cell Dysfunction against High Glucose by Modulating AMPK and NADPH Oxidase Signaling

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 356 ◽  
Author(s):  
Ha-Rim Kim ◽  
Seon-Young Kim
Keyword(s):  
High Glucose ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Cell Damage ◽  
Perilla Frutescens ◽  
Activation Mechanism ◽  
Glomerular Mesangial Cells ◽  
Ampk Activation ◽  
Cell Dysfunction

Perilla frutescens (L.) Britt. var. japonica (Hassk.) Hara (PF), is a medical herb of the Lamiaceae family. We have previously reported that the PF sprout extract (PFSE) is effective in treating hyperglycemia. However, the role of PFSE on glomerular mesangial cells (MCs) proliferation and the extracellular matrix (ECM) accumulation in a diabetic condition are still unclear. Therefore, in this study, we have investigated the role of PFSE on cell proliferation and ECM accumulation in murine glomerular MCs (MMCs), cultured under a high glucose (HG) condition. PFSE treatment attenuated HG-induced MMCs proliferation and hypertrophy. Moreover, the HG-induced ECM protein, collagen IV and fibronectin, overexpression was abolished by the PFFSE treatment. In addition, PFSE inhibited reactive oxygen species (ROS) overproduction and NOX2 and NOX4 expression in MMCs under a HG condition. Our data further revealed the involvement of mesangial cell damage in AMP-activated kinase (AMPK) activation. PFSE strongly activated AMPK in MMCs under hyperglycemic conditions. These results suggest that PFSE inhibits HG-medicated MC fibrosis through suppressing the activation of NOX2/4 and the AMPK activation mechanism. PFSE may be useful for the prevention or treatment of diabetic nephropathy.

scholarly journals Chemoattractants provoke monocyte adhesion to human mesangial cells and mesangial cell injury

1992 ◽  
Vol 42 (2) ◽  
pp. 480-487 ◽  
Author(s):  
Hugh R. Brady ◽  
Mark D. Denton ◽  
Wladimiro Jimenez ◽  
Shoichiro Takata ◽  
Deborah Palliser ◽  
...  
Keyword(s):  
Cell Injury ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Monocyte Adhesion ◽  
Human Mesangial Cells

scholarly journals Protective Effects of Baicalin on Peritoneal Tight Junctions in Piglets Challenged with Glaesserella parasuis

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1268
Author(s):  
Jiacheng Zhang ◽  
Zhaoran Zhang ◽  
Jianfeng Xu ◽  
Chun Ye ◽  
Shulin Fu ◽  
...  
Keyword(s):  
Western Blot ◽  
Protective Effect ◽  
Tight Junctions ◽  
Molecular Mechanisms ◽  
Distribution Patterns ◽  
Protective Effects ◽  
Rt Pcr ◽  
Protective Mechanisms ◽  
Prevention And Treatment ◽  
Natural Agent

Glaesserella parasuis (G. parasuis) causes inflammation and damage to piglets. Whether polyserositis caused by G. parasuis is due to tight junctions damage and the protective effect of baicalin on it have not been examined. Therefore, this study aims to investigate the effects of baicalin on peritoneal tight junctions of piglets challenged with G. parasuis and its underlying molecular mechanisms. Piglets were challenged with G. parasuis and treated with or without baicalin. RT-PCR was performed to examine the expression of peritoneal tight junctions genes. Immunofluorescence was carried out to detect the distribution patterns of tight junctions proteins. Western blot assays were carried out to determine the involved signaling pathways. Our data showed that G. parasuis infection can down-regulate the tight junctions expression and disrupt the distribution of tight junctions proteins. Baicalin can alleviate the down-regulation of tight junctions mRNA in peritoneum, prevent the abnormalities and maintain the continuous organization of tight junctions. Our results provide novel evidence to support that baicalin has the capacity to protect peritoneal tight junctions from G. parasuis-induced inflammation. The protective mechanisms of baicalin could be associated with inhibition of the activation of PKC and MLCK/MLC signaling pathway. Taken together, these data demonstrated that baicalin is a promising natural agent for the prevention and treatment of G. parasuis infection.

scholarly journals Heparin decreases mesangial matrix accumulation after selective antibody-induced mesangial cell injury.

1992 ◽  
Vol 3 (4) ◽  
pp. 921-929
Author(s):  
W W Tang ◽  
C B Wilson
Keyword(s):  
Cell Proliferation ◽  
Cell Injury ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Chronic Administration ◽  
Glomerular Mesangial Cells ◽  
Mesangial Matrix ◽  
Beneficial Effects ◽  
Mesangial Cell Proliferation ◽  
Matrix Accumulation

Anti-rat thymocyte antibody-induced injury of glomerular mesangial cells is characterized initially by lysis (1 h) and is followed by proliferation (beginning at 3 to 4 days), with resolution that can include a focal increase in mesangial matrix (by 28 days). Chronic administration (every 12 h) of heparin (anticoagulant or nonanticoagulant) resulted in a decrease in antibody-induced mesangial cell proliferation, which, in turn, was associated with a decrease in the size and number of areas of focal mesangial matrix increase. The effect could not be attributed to the effect of heparin on complement, to alterations in the small numbers of la-positive cells that characterize the lesion, or to binding of antibody to glomeruli. The beneficial effects of heparin in reducing mesangial cell proliferation, with a subsequent reduction in matrix increase, suggest that mesangial cell responses are a major element in the development of at least some forms of glomerulosclerosis. The possible mechanisms by which these effects of heparin may be achieved are discussed.

scholarly journals The Neuroprotective Effects of Astragaloside IV against H2O2-Induced Damage in SH-SY5Y Cells are Associated with Synaptic Plasticity

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Zurong Song ◽  
Ali Tao
Keyword(s):  
Synaptic Plasticity ◽  
Western Blot ◽  
Cell Viability ◽  
Cell Damage ◽  
Neuroblastoma Cell ◽  
Human Neuroblastoma Cell ◽  
Protective Effects ◽  
Astragaloside Iv ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma

The aim of this study was to investigate whether the neuroprotective effects of astragaloside IV (AS-IV) against hydrogen peroxide (H2O2)-induced damage on human neuroblastoma cell line (SH-SY5Y) are associated with synaptic plasticity. The concentration screening of AS-IV and H2O2 on SH-SY5Y cells and the protective effects of AS-IV on SH-SY5Y cells under H2O2 stress were all determined by MTT assay. The expression of postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were measured by western blot (WB) and inmunofluorescence staining assay under the same treatment conditions. According to the MTT results, the concentration of H2O2 at 50 μmol/L for 3 h was used for the cell damage model, and various concentrations of AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) were used to affect SH-SY5Y cells. The MTT results showed that pretreatment of SH-SY5Y cells with AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) attenuated the damage induced by H2O2 (50 μmol/L, 51.62% cell viability) and increased cell viability to 64.19, 63.48, 65.86, and 65.81%, respectively. Western blot analysis and immunofluorescence staining showed that the protective effects of AS-IV against SH-SY5Y cell damage caused by H2O2 resulted in reduced expression of PSD-95 and increased expression of GAP-43 in comparison with the H2O2 treatment group. The conclusion shows that AS-IV protected SH-SY5Y cells and enhanced their viability under H2O2 stress. AS-IV may facilitate presynaptic and postsynaptic plasticity to exert protective effects against oxidative damage of SH-SY5Y cells.

scholarly journals Cudratricusxanthone O Inhibits H2O2-Induced Cell Damage by Activating Nrf2/HO-1 Pathway in Human Chondrocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 788 ◽  
Author(s):  
Eun-Nam Kim ◽  
Hyun-Su Lee ◽  
Gil-Saeng Jeong
Keyword(s):  
Cell Damage ◽  
Protoporphyrin Ix ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Protective Effects ◽  
Inhibitory Effects ◽  
Ros Accumulation ◽  
Tin Protoporphyrin ◽  
Induced Apoptosis ◽  
Radical Damage

Osteoarthritis (OA) is a common joint degenerative disease induced by oxidative stress in chondrocytes. Although induced-heme oxygenase-1 (HO-1) has been found to protect cells against oxygen radical damage, little information is available regarding the use of bioactive compounds from natural sources for regulating the HO-1 pathway to treat OA. In this study, we explored the inhibitory effects of cudratricusxanthone O (CTO) isolated from the Maclura tricuspidata Bureau (Moraceae) on H2O2-induced damage of SW1353 chondrocytes via regulation of the HO-1 pathway. CTO promoted HO-1 expression by enhancing the translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) into the nucleus without inducing toxicity. Pretreatment with CTO-regulated reactive oxygen species (ROS) production by inducing expression of antioxidant enzymes in H2O2-treated cells and maintained the functions of H2O2-damaged chondrocytes. Furthermore, CTO prevented H2O2-induced apoptosis by regulating the expression of anti-apoptotic proteins. Treatment with the HO-1 inhibitor tin-protoporphyrin IX revealed that these protective effects were exerted due to an increase in HO-1 expression induced by CTO. In conclusion, CTO protects chondrocytes from H2O2-induced damages—including ROS accumulation, dysfunction, and apoptosis through activation of the Nrf2/HO-1 signaling pathway in chondrocytes and, therefore, is a potential therapeutic agent for OA treatment.

scholarly journals Protective Effects of Broussonetia kazinoki Siebold Fruit Extract against Palmitate-Induced Lipotoxicity in Mesangial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Donghee Kim ◽  
Hyo-Jin Kim ◽  
Seon-Heui Cha ◽  
Hee-Sook Jun
Keyword(s):  
Diabetic Nephropathy ◽  
Antioxidant Enzymes ◽  
Protective Effect ◽  
Mesangial Cells ◽  
Ethanolic Extract ◽  
Protective Effects ◽  
Glomerular Mesangial Cells ◽  
Apoptotic Genes ◽  
Stress Related Genes ◽  
Induced Apoptosis

Diabetic nephropathy is one of the most serious complications of diabetes. Lipotoxicity in glomerular mesangial cells is associated with the progression of diabetic nephropathy. Paper mulberry, Broussonetia kazinoki Siebold (BK), has been used in oriental medicine for human health problems. However, to date, the beneficial effect of BK fruit has not been studied. In this study, we investigated the protective effect of an ethanolic extract of BK fruit (BKFE) against palmitate- (PA-) induced toxicity in mesangial cells. BKFE significantly increased the viability of PA-treated SV40 MES13 cells. BKFE significantly inhibited PA-induced apoptosis and decreased the expression of apoptotic genes, cleaved caspase-3, and cleaved PARP. Moreover, BKFE inhibited the expression of endoplasmic reticulum (ER) stress-related genes, such as BiP, phosphorylated eIF2α, cleaved ATF6, and spliced XBP-1, in PA-treated SV40 MES13 cells. BKFE decreased PA-induced ROS production. In addition, BKFE activated the transcription factor Nrf2 and increased the expression of antioxidant enzymes. However, knockdown of Nrf2 using siRNA suppressed this BKFE-induced increase in antioxidant enzyme expression. Furthermore, the protective effect of BKFE on PA-induced apoptosis was significantly reduced by Nrf2 knockdown. In conclusion, BKFE induced the expression of antioxidant enzymes via activation of Nrf2 and protected against PA-induced lipotoxicity in mesangial cells.

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