scholarly journals Protective Effect of a Novel Polysaccharide from Lonicera japonica on Cardiomyocytes of Mice Injured by Hydrogen Peroxide

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Xiaonan Zhou ◽  
Gui He ◽  
Jinming Ma ◽  
Min Tang ◽  
Geng Tian ◽  
...  

Lonicera japonica is a traditional Chinese herbal medicine with antioxidation, anti-inflammatory, antibacterial, and immunoregulation functions. A method to isolate polysaccharides from Lonicera japonica (LJP) has been reported previously by our group. We also reported previously that LJP was consisted of 6 types of monosaccharides and had the characteristic absorption of typical polysaccharides. In this study, we investigated the protective effect of LJP on cardiomyocytes of mice injured by hydrogen peroxide (H2O2). The results showed that LJP can increase the cardiomyocyte viability and the activities of the enzyme (SOD, CAT, GSH-Px, AST, CPK, and LDH) in cardiomyocytes of mice injured by hydrogen peroxide. The results of intracellular ROS contents showed that a high dose (40 μg mL-1) of LJP had the best effects on protecting the cardiomyocytes of mice injured by H2O2. In addition, the measurement results of the cardiomyocyte apoptosis and the activity of caspase-3, caspase-8, and caspase-9 in cardiomyocytes confirmed this conclusion from another perspective.

Perfusion ◽  
2022 ◽  
pp. 026765912110599
Author(s):  
Wenling Li ◽  
Hua Sang ◽  
Xin Xu ◽  
Yuanyuan Zhang ◽  
Xiangying Meng ◽  
...  

Objective Dihydromyricetin (DMY), also called Ampelopsin, which was extracted from Ampelopsis grossedentata, has been demonstrated to have a protective effect against cell oxidative injury and cell apoptosis in vitro. In the present study, we tried to study the role of DMY on apoptosis of vascular smooth muscle cells (VSMCs) induced by hydrogen peroxide (H2O2) and explore the underlying mechanisms. Methods Apoptotic cells were detected by Hematoxylin and Eosin (H.E.) staining, Hoechst 33342 staining, and Annexin V-fluorescein isothiocyanate binding assay. The intracellular reactive oxygen species (ROS) level was estimated through fluorescence assay. The mRNA and protein expression of Caspase-3, Caspase-9, Bcl-2, and Bax were determined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Results The results showed that the pretreatment of VSMCs with DMY not only significantly increased cell viability, reduced intracellular ROS release, alleviated the morphological changes of apoptosis, and decreased the apoptosis rate, but also upregulated Bcl-2 expression and downregulated Caspase-3, Caspase-9, Bax expression, and ultimately attenuated the H2O2-stimulated apoptosis. Conclusion The inhibition of DMY on VSMC apoptosis may be mediated by ROS scavenging and the activation of the mitochondrial apoptotic signaling pathway.


2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Marwa M. M. Refaie ◽  
Entesar F. Amin ◽  
Nashwa F. El-Tahawy ◽  
Aly M. Abdelrahman

Nephrotoxicity is one of the limiting factors for using doxorubicin (DOX). Interleukin 1 has major role in DOX-induced nephrotoxicity, so we investigated the effect of interleukin 1 receptor antagonist diacerein (DIA) on DOX-induced nephrotoxicity. DIA (25 and 50 mg/kg/day) was administered orally to rats for 15 days, in the presence or absence of nephrotoxicity induced by a single intraperitoneal injection of DOX (15 mg/kg) at the 11th day. We measured levels of serum urea, creatinine, renal reduced glutathione (GSH), malondialdehyde (MDA), total nitrites (NOx), catalase, and superoxide dismutase (SOD). In addition, caspase-3, tumor necrosis factor alpha (TNFα), nuclear factor kappa B (NFκB) expressions, and renal histopathology were assessed. Our results showed that DOX-induced nephrotoxicity was ameliorated or reduced by both doses of DIA, but diacerein high dose (DHD) showed more improvement than diacerein low dose (DLD). This protective effect was manifested by significant improvement in all measured parameters compared to DOX treated group by using DHD. DLD showed significant improvement of creatinine, MDA, NOx, GSH, histopathology, and immunohistochemical parameters compared to DOX treated group.


Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5818
Author(s):  
Shengnan Zhu ◽  
Jicheng Xu ◽  
Huizhi Chen ◽  
Weiqiao Lv

Prunus mume blossom is an edible flower that has been used in traditional Chinese medicine for thousands of years. Flavonoids are one of the most active substances in Prunus mume blossoms. The optimal ultrasonic-assisted enzymatic extraction of flavonoids from Prunus mume blossom (FPMB), the components of FPMB, and its protective effect on injured cardiomyocytes were investigated in this study. According to our results, the optimal extraction process for FPMB is as follows: cellulase at 2.0%, ultrasonic power at 300 W, ultrasonic enzymolysis for 30 min, and an enzymolysis temperature of 40 °C. FPMB significantly promoted the survival rate of cardiomyocytes and reduced the concentration of reactive oxygen species (ROS). FPMB also improved the activities of proteases caspase-3, caspase-8, and caspase-9 in cardiomyocytes. The cardiomyocyte apoptosis rate in mice was significantly reduced by exposure to FPMB. These results suggest that the extraction rate of FPMB may be improved by an ultrasonic-assisted enzymatic method. FPMB has a protective effect on the injured cardiomyocytes.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jing Wang ◽  
Zhichun Dong ◽  
Liyin Lou ◽  
Lijuan Yang ◽  
Jingying Qiu

At present, there are few reports concerning the relationship between miR-122 and diabetes. In addition, the effect of miR-122 on streptozotocin- (STZ-) induced oxidative damage in INS-1 cells remains unclear. The present study aimed to investigate the role and modulatory mechanisms involving miR-122 in diabetes. STZ was used to induce INS-1 cell damage. Reverse transcription-quantitative PCR was used to investigate the expression of miR-122. A TUNEL cell apoptosis detection kit was used to detect apoptosis. Intracellular ROS levels were determined using dichlorofluorescein-diacetate. The activities of insulin secretion, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-px) were measured using ELISA kits. Western blotting was used to measure the expression levels of Bax, Bcl-2, PI3K, p-PI3K, caspase-3 and caspase-9, cleaved-caspase-3 and cleaved-caspase-9, AKT, and p-AKT. Then, LY294002 (LY, PI3K inhibitor) was used to treat INS-1 cells, and oxidative stress and apoptosis were measured. The results showed that STZ-induced inhibitory effects on insulin secretion were mitigated by miR-122 inhibitor, and the activities of SOD, CAT, and GSH-px were also increased. Furthermore, miR-122 inhibitor inhibited apoptosis and oxidative stress in STZ-induced INS-1 cells. Finally, the addition of LY increased insulin levels; reduced the activities of SOD, CAT, and GSH-px; and promoted apoptosis in STZ-induced INS-1 cells. In conclusion, interference with miR-122 can inhibit oxidative stress and apoptosis in STZ-induced INS-1 cells, involving a mechanism of action related to the PI3K/AKT pathway.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Kuo-Jen Wu ◽  
Yuh-Fung Chen ◽  
Huei-Yann Tsai ◽  
Chi-Rei Wu ◽  
W. Gibson Wood

Brain neuronal apoptosis and cognitive impairment are associated with hyperglycemia and diabetes mellitus. The present study determined if the Chinese herbal medicineGuizhi-Fuling-Wan(GFW) would reduce memory loss and neuronal apoptosis in streptozotocin- (STZ-) induced hyperglycemic rodents. Two weeks after STZ induction, GFW was orally administered once daily for 7 days. GFW significantly improved spatial memory deficits in STZ-induced hyperglycemic mice. GFW decreased TUNEL-positive cells and caspase-3 positive cells in STZ-induced hyperglycemic rats. It also was found that GFW treatment reduced caspase-3 protein levels and increased levels of the antiapoptotic protein Bcl-2 that were indicative of neuroprotection. The protective therapeutic effects of GFW on neuronal apoptosis and cognition deficits caused by STZ-induced hyperglycemia may be due in part to inhibition of the cellular apoptosis pathway. GFW may have therapeutic effects in patients with diabetes-mellitus-induced neuropathology.


2021 ◽  
Author(s):  
FAHRIYE ZEMHERI NAVRUZ ◽  
Sinan INCE ◽  
Damla ARSLAN-ACAROZ ◽  
Ulaş ACAROZ ◽  
Hasan Hüseyin DEMIREL ◽  
...  

Abstract Pyraclostrobin (Pyra) is a fungicide in the strobilurin class and has proven to be very toxic to aquatic species. Resveratrol (Res) is a phytoalexin that exhibits multiple bioactivities as antioxidative, anti-inflammatory, cardiovascular protective, and anti-aging in animals and is found in plant species such as mulberry, peanut, and grape. This study aimed to determine the protective effect of Res against Pyra-induced oxidative stress in rats. For this purpose, a total of 48 male rats divided into 6 groups − 8 in each group - were exposed to 30 mg/kg Pyra by oral gavage once a day for 4 weeks and to 3 different concentrations of Res (5, 10 and 20 mg/kg) together with Pyra. It was observed that, in groups administered with Pyra, malondialdehyde (MDA) levels increased whereas glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels decreased. It was observed that, in the group administered with Pyra, expression levels of CYP2E1 gene, which is associated with increased cancer risk, pro-apoptotic BAX gene, apoptotic caspase-3, caspase-8 and caspase-9 genes, NFκB gene, which is a pro-inflammatory transcription factor, and p53 gene, which plays a regulatory role in the cell, increased whereas expression level of anti-apoptotic bcl-2 gene decreased. It was determined that Res administrations improved Pyra-induced oxidative damage, histopathological changes and expression levels of various genes. According to the ssDNA analysis obtained from the DNA isolated from the blood; when DNA damage and histopathological damage in tissues were examined, it was observed that the highest damage was in the group administered with Pyra and the damage decreased depending on the increase in dose of Res. Consequently, it was observed that Res, known for its antioxidant protective properties, exhibited a protective effect against oxidative stress caused by Pyra.


2021 ◽  
Vol 19 ◽  
pp. 205873922110511
Author(s):  
Mirensha Yakufu ◽  
Renaguli Hailiwu ◽  
Yuanyuan Cong ◽  
Ayijiang Habaike ◽  
Xiaomei Wang ◽  
...  

Introduction: To investigate antitumor activity and mechanism of flavonoids from Alpinia officinarum Hance against gastric cancer. Methods: Transplanted mouse fore-stomach carcinoma (MFC) tumor mice were divided into six groups: control group, model group, low dose (20 mg/kg), middle dose (40 mg/kg), and high dose (80 mg/kg) groups of TFAO and 5-Fu group. Mice were treated with TFAO or 5-Fu for 14 days, except those of control and model group. Tumor inhibitory rate, spleen, and thymus index were calculated. Contents of proliferating cell nuclear antigen, MMP-9, vascular endothelial growth factor, IL-1β, IL-6, and IL-17 in serum were detected. Effect of galangin on BGC-823 cell growth was detected. Cell apoptosis and cell cycle distribution were measured. Enzyme activity of Caspase-3, Caspase-8, and Caspase-9 was detected. Western blot was used to detect STAT3, Bcl-2, Bax, Caspase-3, Caspase-8, Caspase-9, CyclinB1, and CyclinD1 protein expression in BGC-823 cell. Results: Compared with model group, tumor weight of mice decreased significantly ( p < .01) in 5-Fu group, low dose, middle dose, and high dose group of TFAO; thymus index of mice decreased significantly ( p < .05) in 5-Fu group; and spleen index decreased significantly ( p < .05) in low dose and middle dose groups of TFAO. Compared with model group, levels of PCNA, MMP-9, IL-1β, and IL-6 in serum of mice decreased obviously ( p < .01) in all administration groups; levels of VEGF in serum of mice decreased obviously ( p < .01) in low dose and high dose group of TFAO and 5-Fu group; and levels of IL-17 in serum of mice decreased significantly ( p < .01) in low-dose and middle-dose groups of TFAO and 5-Fu group. Galangin could inhibit BGC-823 cell growth; accelerate apoptosis; block cell cycle; increase cell Caspase-3, Caspase-8, and Caspase-9 enzyme activity; upregulate expression of Caspase-3, Caspase-8, Caspase-9, and Bax; and downregulate expression of STAT3, CyclinB1, CyclinD1, and Bcl-2 protein. Conclusion: Flavonoids from A. officinarum showed antitumor activity in gastric cancer. Mechanisms may be associated with inhibition of tumor angiogenesis, tumor cell proliferation, and cancer-associated inflammation.


2019 ◽  
Vol 20 (3) ◽  
pp. 754 ◽  
Author(s):  
Zhihang Yuan ◽  
Zengenni Liang ◽  
Jine Yi ◽  
Xiaojun Chen ◽  
Rongfang Li ◽  
...  

Medicinal herbal plants have been commonly used for intervention in different diseases and improvement of health worldwide. Koumine, an alkaloid monomer found abundantly in Gelsemium plants, can be effectively used as an antioxidant. The purpose of this study was to evaluate the potential protective effect of koumine against hydrogen peroxide (H2O2)-induced oxidative stress and apoptosis in porcine intestinal epithelial cell line (IPEC-J2 cells). MTT assays showed that koumine significantly increased cell viability in H2O2-mediated IPEC-J2 cells. Preincubation with koumine ameliorated H2O2-medicated apoptosis by decreasing reactive oxygen species (ROS) production, and efficiently suppressed the lactate dehydrogenase (LDH) release and malondialdehyde (MDA) production. Moreover, a loss of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) activities was restored to normal level in H2O2-induced IPEC-J2 cells upon koumine exposure. Furthermore, pretreatment with koumine suppressed H2O2-mediated loss of mitochondrial membrane potential, caspase-9 and caspase-3 activation, decrease of Bcl-2 expression and elevation of Bax expressions. Collectively, the results of this study indicated that koumine possesses the cytoprotective effects in IPEC-J2 cells during exposure to H2O2 by suppressing production of ROS, inhibiting the caspase-3 activity and influencing the expression of Bax and Bcl-2. Koumine could potentially serve as a protective effect against H2O2-induced apoptosis.


2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Dan Luo ◽  
Zhipeng Peng ◽  
Le Yang ◽  
Mingren Qu ◽  
Xiaowen Xiong ◽  
...  

The effects and underlying mechanisms of butyrate and butyrate+niacin on apoptosis in sheep rumen epithelial cells were investigated. Cells were exposed to butyrate (0–140 mM) for 6 h. A low concentration (20 mM) of butyrate increased cell viability and promoted growth whereas high concentrations (40–140 mM) inhibited proliferation. Cells were then cocultured with 120 mM butyrate and niacin (0–100 mM) for 6 h. Niacin addition attenuated butyrate-induced cellular damage and promoted proliferation at 20–80 mM; 40 mM presented the optimal effect. Higher concentrations (100 mM) of niacin resulted in low cell viability. Subsequent experiments confirmed that 120 mM butyrate increased intracellular reactive oxygen species (ROS) production and reduced the intracellular total antioxidant capacity (T-AOC) versus the untreated control. Compared with 120 mM butyrate, cotreatment with 40 mM niacin significantly reduced the intracellular ROS content and increased the intracellular T-AOC. Flow cytometry analysis revealed that 120 mM butyrate increased the proportion of apoptotic cells by 17.8% versus the untreated control, and 120 mM butyrate+40 mM niacin treatment reduced the proportion of apoptotic cells by 28.6% and 39.4% versus the untreated control and butyrate treatment, respectively. Treatment with 120 mM butyrate increased caspase-9 and p53 mRNA levels and decreased the expression of Bcl-2 and Bax, and the Bcl-2/Bax ratio versus the untreated control. Treatment with 120 mM butyrate+40 mM niacin downregulated the expression of caspase-3 and p53 and increased the expression of Bcl-2 and Bax versus butyrate treatment alone but had no effect on the Bcl-2/Bax ratio. Thus, high concentrations of butyrate may induce rumen epithelial cell apoptosis by increasing oxidative stress and inducing caspase-9 and p53 expression. Cotreatment with niacin regulates apoptosis-related gene expression by reducing intracellular ROS production and DNA damage and downregulating caspase-3 and p53 expressions to protect rumen epithelial cells against butyrate-induced apoptosis.


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