Effect of Reynoutria Japonica and its Extract on Sirt1 in Cisplatin-Induced Renal Injury

2021 ◽  
Author(s):  
Shangmei Cao ◽  
Xiaojing Liu ◽  
Xinxin sun ◽  
Xixia Chen ◽  
Shuifu Tang
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Protein Expression ◽  
Kidney Injury ◽  
Model Group ◽  
Drug Induced ◽  
Blank Group ◽  
Reynoutria Japonica ◽  
Gene And Protein Expression ◽  
Sirt1 Gene

Abstract Background: Mechanisms of drug-induced kidney injury include mitochondrial dysfunction and oxidative stress. Resveratrol is a natural activator of sirt1 that is related to oxidative stress.Aim: To explore the mechanism of treating drug-induced kidney injury with Reynoutria japonica and its extract (Resveratrol).Design: Fifty adult male SD rats were randomly divided into five groups: blank group, model group, Reynoutria japonica group, resveratrol group and lotensin group. Each group was given the corresponding drug. ACR was measured on the seventh day every week. Creatinine and urea nitrogen were measured on the fourth weekend. All rats were sacrificed on the fourth weekend to detect the relevant indicators in the kidney.Results: At the fourth week, the ACR, Scr and BUN of the Resveratrol group were higher than those of the lotensin group and Reynoutria japonica group (P<0.05). The values of Scr and BUN were lower in the Reynoutria japonica group than in the lotensin group (P<0.05). The levels of SOD, NO, and sirt1 gene and protein expression in the model group and treatment group were lower than those in the blank group, and those in the model group were lower than those in the treatment group (P<0.05). The levels of SOD, NO, and sirt1 gene and protein expression in the Reynoutria japonica group were higher than the lotensin group (P<0.05).Conclusions: The therapeutic effect of the Reynoutria japonica group was better than that of the lotensin group and resveratrol group.

scholarly journals Effect of Reynoutria Japonic and Resveratrol on Sirt1/SOD/MDA of Adriamycin-Induced Renal Injury: A Randomised Trial

2021 ◽  
Author(s):  
Shangmei Cao ◽  
xiaojing liu ◽  
xinxin sun ◽  
xixia chen ◽  
shuifu Tang
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Injury ◽  
Group Model ◽  
Mrna Levels ◽  
Model Group ◽  
Drug Induced ◽  
Blank Group ◽  
Reynoutria Japonica ◽  
Comparison Results

Abstract Background: Mechanisms of drug-induced kidney injury include mitochondrial dysfunction and oxidative stress. Resveratrol is a natural activator of sirt1 that is related to oxidative stress.Objectives: To explore the mechanism of treating drug-induced kidney injury with Reynoutria japonica and its extract (Resveratrol).Methods: Fifty adult male SD rats were randomly divided into five groups: blank group, model group, Reynoutria japonica group, resveratrol group and Benazepril group. Except the blank group, each group used a one-time tail vein injection of 7.5mg/kg adriamycin to make the rat model of drug-induced renal injury. After three days, the proteinuria test strip showed green, which was positive for proteinuria. Each group was given the corresponding drug. ACR was measured on the seventh day every week. All rats were anaesthetized death on the fourth weekend to obtain blood and kidneys. Results: At the fourth week, the MDA levels of blank group and Reynoutria japonica group were significantly lower than those of benazepril hydrochloride group (P<0.05), and the MDA levels of resveratrol group and model group were significantly higher than those of benazepril hydrochloride group (P<0.05).The Sirt1 mRNA levels of the blank group and the Reynoutria japonica group were significantly higher than those in the benazepril hydrochloride group (P<0.05), and the Sirt1 mRNA levels of resveratrol group and model group were significantly lower than those of the benazepril hydrochloride group (P<0.05). The comparison results between groups of the Sirt1 protein expression were the same as those of the Sirt1 mRNA expression (P<0.05).Conclusions: The therapeutic effect of the Reynoutria japonica group was better than that of the Benazepril group and resveratrol group.

scholarly journals CircRNA expression profiles in human dental pulp stromal cells undergoing oxidative stress

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Jingying Zhang ◽  
Dan Li ◽  
Dan Wang ◽  
Kenny Man ◽  
Xuebin Yang
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Stromal Cells ◽  
Dental Pulp ◽  
Kegg Pathway ◽  
Global Changes ◽  
Qrt Pcr ◽  
Gene And Protein Expression ◽  
Human Dental Pulp ◽  
Sirt1 Gene

Abstract Background Oxidative stress has a determinantal effect on human dental pulp stromal cells (hDPSCs), including affecting their longevity and functionality. Circular RNAs (circRNAs) play an essential role in stromal cell behavior; however, the exact mechanism in which circRNAs functions within hDPSCs were undergoing oxidative stress remains unclear. The purpose of this study is to assess the global changes and characteristics of circRNAs in hDPSCs undergoing oxidative stress. Methods Using an oxidative stress model of hDPSCs, we applied microarray analysis to examine the circRNAs profiles. We confirmed the changes in circRNAs by quantitative Real-Time PCR (qRT-PCR). Furthermore, bioinformatics tools, including a miRcode map, TargetScan, gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, were reconstructed for further assessment. SIRT1 gene and protein expression were tested by qRT-PCR and In Cell-Western analysis. Results We revealed 330 upregulated, and 533 downregulated circRNAs undergoing oxidative stress in hDPSCs and confirmed three circRNAs distinct expressions (hsa_circ_0000257, hsa_circ_0087354, and hsa_circ_0001946) in hDPSCs undergoing oxidative stress by qRT-PCR. GO, and KEGG pathway enrichment revealed the differentially expressed circRNAs might participate in p53 and cell cycle signaling networks associated with oxidative stress. SIRT1 gene and protein expression was reduced in the oxidatively stressed cells (OSC) group compared to untreated cells (UC). Conclusions The findings of this study has provided new insights into circRNAs and a basis for further studies assessing the potential functions of hsa_circ_0000257, hsa_circ_0087354, and hsa_circ_0001946 in oxidatively stressed hDPSCs.

scholarly journals PO-086 Exercise enhances cardiac antioxidant capacity in diabetic rats through the Keap1/Nrf2 signaling pathway

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Shiqiang Wang
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Diabetic Rats ◽  
Heart Weight ◽  
Stress Injury ◽  
Myocardial Oxidative Stress ◽  
Nrf2 Signaling Pathway ◽  
Gene And Protein Expression

Objective To investigate the effects of exercise on the myocardial oxidative stress injury of diabetic rats, and discussed the role of Keap1/Nrf2 signaling pathway in this process Methods  Tyep 2 diabetic rat model was established by streptozotocin injection through abdominal cavity and high fat diet. The all the diabetic rats were divided into three groups: control group (NC), diabetes group(T2DM) and diabetes exercise group, NC and T2DM group were kept quiet for 8 weeks, T2DME group was trained for 8 weeks. After the exercise, weight, heart weight and blood were measured. MDA, T-SOD and GSH-PX enzyme were measured by biochemical method. Ho-1, Keap1, Nrf2 gene and protein expression were detected by RT-PCR and WesternBlotting. Results Compared with NC group, the weight of rats in the T2DM group significantly decreased [(528+/-71g vs 362+/-33g), P<0.05], HWI  significantly increased [(2.845+/-0.22 vs 3.841+/-0.21, P <0.05], blood glucose was significantly increased [(6.4±3.8 vs 26±7.5mmol/L), P <0.01],T-SOD and GSH-PX activity decreased significantly (P<0.05), Ho-1 protein expression increased (P<0.01), Keap1 and Nrf2 showed no significant changes, and Nrf2 nuclear transposition decreased (P<0.05). Compared with the T2DM group, no significant change in body weight and heart weight in the T2DME group, with significant decrease in HWI[（3.841±0.21 vs 3.235±0.23），P＜0.05], with significant decrease in blood glucose [（26.0±7.5 vs 21.0±6.8），P＜0.05]. Ho-1 gene and protein expression increased significantly（P＜0.05and P＜0.01）, with no significant change of Keap1, while Nrf2 expression increased significantly (P < 0.05), and Nrf2 nuclear transposition increased significantly (P < 0.01). Conclusions Exercise activates the myocardial Keap1/Nrf2 signaling pathway in rats, promotes the expression of downstream antioxidant enzymes, increases cardiac antioxidant capacity, and resists diabetic myocardial oxidative stress injury.

scholarly journals Antioxidant Activity, Phenolic Profile, and Nephroprotective Potential of Anastatica hierochuntica Ethanolic and Aqueous Extracts against CCl4-Induced Nephrotoxicity in Rats

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2973
Author(s):  
Tariq I. Almundarij ◽  
Yousef M. Alharbi ◽  
Hassan A. Abdel-Rahman ◽  
Hassan Barakat
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Therapeutic Agent ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Total Phenolic ◽  
Drug Induced ◽  
Total Carotenoids ◽  
Phenolic Profile ◽  
Better Than

Kaff-e-Maryam (Anastatica hierochuntica L.) is extensively used to treat a range of health problems, most notably to ease childbirth and alleviate reproductive system-related disorders. This study aimed to evaluate the effect of A. hierochuntica ethanolic (KEE), and aqueous (KAE) extracts on CCl4-induced oxidative stress and nephrotoxicity in rats using the biochemical markers for renal functions and antioxidant status as well as histopathological examinations of kidney tissue. A. hierochuntica contained 67.49 mg GAE g−1 of total phenolic compounds (TPC), 3.51 µg g−1 of total carotenoids (TC), and 49.78 and 17.45 mg QE g−1 of total flavonoids (TF) and total flavonols (TFL), respectively. It resulted in 128.71 µmol of TE g−1 of DPPH-RSA and 141.92 µmol of TE g−1 of ABTS-RSA. A. hierochuntica presented superior antioxidant activity by inhibiting linoleic acid radicals and chelating oxidation metals. The HPLC analysis resulted in 9 and 21 phenolic acids and 6 and 2 flavonoids in KEE and KAE with a predominance of sinapic and syringic acids, respectively. Intramuscular injection of vit. E + Se and oral administration of KEE, KAE, and KEE + KAE at 250 mg kg−1 body weight significantly restored serum creatinine, urea, K, total protein, and albumin levels. Additionally, they reduced malondialdehyde (MOD), restored reduced-glutathione (GSH), and enhanced superoxide dismutase (SOD) levels. KEE, KAE, and KEE + KAE protected the kidneys from CCl4-nephrotoxicity as they mainly attenuated induced oxidative stress. Total nephroprotection was about 83.27%, 97.62%, and 78.85% for KEE, KAE, and KEE + KAE, respectively. Both vit. E + Se and A. hierochuntica extracts attenuated the histopathological alteration in CCl4-treated rats. In conclusion, A. hierochuntica, especially KAE, has the potential capability to restore oxidative stability and improve kidney function after CCl4 acute kidney injury better than KEE. Therefore, A. hierochuntica has the potential to be a useful therapeutic agent in the treatment of drug-induced nephrotoxicity.

scholarly journals Fasudil ameliorated liposaccharide-induced acute kidney injury in mice by inhibiting NLRP3

2021 ◽  
Vol 20 (10) ◽  
pp. 2055-2062
Author(s):  
Xueqian Li ◽  
Chengzhi Zhao
Keyword(s):  
Acute Kidney Injury ◽  
Treatment Group ◽  
Cell Growth ◽  
Mesangial Cells ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Control Group ◽  
Model Group ◽  
Blank Control Group ◽  
Tissue Homogenates

Purpose: To determine the influence of fasudil on LPS-mediated acute kidney injury (AKI) in mice.Methods: Healthy C57 mice (n = 140) of largely similar weight were used in this study. They were assigned to a treatment group (n = 40), a model group (n = 50), and a blank control group (n = 50). Mice in treatment and model groups were injected with lipopolysaccharide (LPS). In the treatment group, each mouse was injected intravenously with fasudil daily before the establishment of the mouse model of AKI. All mice were sacrificed 6 h after establishing the AKI model. Portions of the kidney from mice were used for preparation of tissue homogenates, while the remaining portions were subjected to primary culture. Transformed C3H Mouse Kidney-1 (TCMK1) and mesangial cells from mouse glomeruli (SV40-MES-13) cells were used for assays of cell growth and apoptosis. Blood samples were alsocollected from the mice. Thereafter, the levels of blood urea nitrogen (BUN) and creatinine (Cr) in kidney homogenates of the three groups were determined. Moreover, levels of NLRP3, nuclear factor kappa-B (NF-κB), toll-like receptor 4 (TLR4), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β in the homogenates and blood were assayed. Cell growth and apoptosis were also measured.Results: The treatment group and model group showed higher levels of BUN and Cr than the control group, with a higher level observed in model mice than in the treatment mice. There were significantly higher relative levels of NF-κB, NLRP3 and TLR4 in treatment and model groups than in controls, with a higher level observed in model mice than in treatment mice. There were significantly higher concentrations of inflammatory factors in treatment and model mice groups than in control mice, with higher levels observed in model mice than in treatment mice. The TCMK1 and SV40-MES-13 cells in the two groups showed slower cell growth and stronger apoptosis than those in control group (p < 0.05).Conclusion: Fasudil relieved LPS-mediated AKI in mice by suppressing TLR4/NF-κB signal pathway and lowering NLRP3. Thus, fasudil has potential as a new adjunctive agent for the treatment of AKI.

scholarly journals Structural Characterization and Antioxidant Activity of Polysaccharides from Athyrium multidentatum (Doll.) Ching in d-Galactose-Induced Aging Mice via PI3K/AKT Pathway

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3364 ◽  
Author(s):  
Liang Jing ◽  
Jing-Ru Jiang ◽  
Dong-Mei Liu ◽  
Ji-Wen Sheng ◽  
Wei-Fen Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Weight ◽  
Protein Expression ◽  
Mrna Expression ◽  
Caspase 3 ◽  
Akt Pathway ◽  
Protective Mechanism ◽  
Related Factor ◽  
Bax Protein ◽  
Gene And Protein Expression

The purpose of this study was to characterize the polysaccharides from Athyrium multidentatum (Doll.) Ching (AMC) rhizome and explore the protective mechanism against d-galactose-induced oxidative stress in aging mice. Methods: A series of experiments, including molecular weight, monosaccharide composition, Fourier transform infrared (FT-IR) spectroscopy, and 1H nuclear magnetic resonance (1H NMR) spectroscopy were carried out to characterize AMC polysaccharides. The mechanism was investigated exploring d-galactose-induced aging mouse model. Quantitative real-time reverse transcription polymerase chain reaction (RT-qPCR) and western blotting assays were performed to assess the gene and protein expression in liver. Key findings: Our results showed that AMC polysaccharides were mainly composed of mannose (Man), rhamnose (Rha), glucuronic acid (Glc A), glucose (Glc), galactose (Gal), arabinose (Ara), and fucose (Fuc) in a molar ratio of 0.077:0.088:0.09:1:0.375:0.354:0.04 with a molecular weight of 33203 Da (Mw). AMC polysaccharides strikingly reversed d-galactose-induced changes in mice, including upregulated phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor-erythroid 2-related factor 2 (Nrf2), forkhead box O3a (FOXO3a), and hemeoxygenase-1 (HO-1) mRNA expression, raised Bcl-2/Bax ratio, downregulated caspase-3 mRNA expression, enhanced Akt, phosphorylation of Akt (p-Akt), Nrf2 and HO-1 protein expression, decreased caspase-3, and Bax protein expression. Conclusion: AMC polysaccharides attenuated d-galactose-induced oxidative stress and cell apoptosis by activating the PI3K/AKT pathway, which might in part contributed to their anti-aging activity.

Methylphenidate causes cytotoxicity on photoreceptor cells via autophagy

2020 ◽  
Vol 40 (1) ◽  
pp. 71-80
Author(s):  
N Kong ◽  
Y Bao ◽  
H Zhao ◽  
X Kang ◽  
X Tai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Messenger Rna ◽  
Cell Damage ◽  
Photoreceptor Cells ◽  
Cell Toxicity ◽  
Hyperactivity Disorder ◽  
Increased Risk ◽  
Gene And Protein Expression ◽  
Underlying Mechanisms

Methylphenidate (MPH) is used as the first-line treatment for attention-deficit hyperactivity disorder. However, there are concerns that this treatment may be associated with increased risk of retinal damage. This study was to investigate cytotoxicity of MPH on photoreceptor cells and explore its underlying mechanisms. MPH-caused cell toxicity was established in 661 W cells. Cytotoxicity was evaluated by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium-bromid and lactate dehydrogenase assays. Oxidative stress was measured by the markers: glutathione (GSH) reductase, catalase, and superoxide dismutase activities as well as GSH, reactive oxygen species, and malondialdehyde levels. Gene and protein expression was detected by real-time polymerase chain reaction (PCR) and western blot, respectively. Results showed that MPH decreased 661 W cell viability, increased caspase-3/9 activities, and induced oxidative stress. Furthermore, MPH treatment increased messenger RNA (mRNA) expression of Beclin-1 and microtubule-associated protein 1A/1B-light chain 3B (LC3B) protein expression in 661 W cells, suggesting autophagy was induced. MPH treatment also upregulated p-JAK1/p-STAT1 protein expression. These data demonstrated that MPH could increase oxidative stress in photoreceptor cells to cause cell toxicity via autophagy, providing the scientific rationale for the photoreceptor cell damage caused by the MPH administration.

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