Alfalfa saponins plays protective roles in oxidative stress-induced apoptotic cells

2020 ◽  
Author(s):  
Yalei Cui ◽  
Boshuai Liu ◽  
Xiao Sun ◽  
Zidan Li ◽  
Yanyan Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Feed Additive ◽  
Drug Candidate ◽  
Protective Mechanism ◽  
Intestinal Epithelial ◽  
Study Results ◽  
New Strategy ◽  
Antioxidant Effects

Abstract Background: As is known, alfalfa saponin can be used as a feed additive in the pig’s diet. And the addition of alfalfa saponin to the pig’s diet could improve animal antioxidant capacity. However, the mechanism by which alfalfa saponins exerts their antioxidant effects has not been studied. To address this issue, H2O2-induced rat intestinal epithelial cell was used to explore the protective mechanism of alfalfa saponins in this study. Results: Alfalfa saponin could rescue the cell proliferation activity, elevate the amount of antioxidant enzymes and downregulate the release of MDA and LDH in H2O2-induced cells. The results indicated that the antioxidant activity of alfalfa saponin was achieved by restoring GSH homeostasis. Further results demonstrated that alfalfa saponin could inhibit cell apoptosis through activating MAPK signaling pathway. Conclusions: The mechanism by which alfalfa saponins exerts their antioxidant effects was elucidated. Therefore, alfalfa saponin could function as cellular oxidative damage inhibitor, green feed additive or potential drug candidate, providing new strategy for inhibiting cell apoptosis induced by oxidative stress in monogastric animals.

scholarly journals Schisandrin A protects intestinal cells from mycophenolic acid-induced cytotoxicity and oxidative damage

2021 ◽  
Author(s):  
Yiyun Deng ◽  
Zhe Zhang ◽  
Yuanyuan Hong ◽  
Lijuan Feng ◽  
Yong Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Mycophenolic Acid ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Mapk Signaling ◽  
Intestinal Epithelial

Abstract Objectives: The gastrointestinal side effects of mycophenolic acid affect its efficacy in kidney transplant patients, which may be due to its toxicity to the intestinal epithelial mechanical barrier, including intestinal epithelial cell apoptosis and destruction of tight junctions. The toxicity mechanism of mycophenolic acid is related to oxidative stress-mediated the activation of mitogen-activated protein kinases (MAP K). Schisandrin A (Sch A), one of the main active components of the Schisandra chinensis, can protects intestinal epithelial cells from deoxynivalenol-induced cytotoxicity and oxidative damage by antioxidant effects. The aim of this study was to investigate the protective effect and potential mechanism of Sch A on mycophenolic acid-induced damage in intestinal epithelial cell. Methods: Caco-2 cells monolayers were treated with mycophenolic acid (10µM) and/or Sch A (10, 20 and 40µM) at 37°C for 24h, and cell viability was measured by MTT; Western blot and immunofluorescence were used to detect the expression of relevant proteins. Intracellular ROS and apoptosis were measured by flow cytometry, and malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by kits. Results: The results showed that Sch A significantly reversed the mycophenolic acid-induced cell viability reduction, restored the expression of tight junction protein ZO-1, occludin and reduced cell apoptosis. In addition, Sch A inhibited mycophenolic acid-mediated MAPK activation and reactive oxygen species (ROS) increase. Conclusions: Sch A protected intestinal epithelial cells from mycophenolic acid intestinal toxicity, at least in part, by reducing oxidative stress and inhibiting MAPK signaling pathway. Conclusions: Sch A protected intestinal epithelial cells from mycophenolic acid intestinal toxicity, at least in part, by reducing oxidative stress and inhibiting MAPK signaling pathway.

scholarly journals Protective Effect of Penetratin Analogue-Tagged SOD1 on Cisplatin-Induced Nephrotoxicity through Inhibiting Oxidative Stress and JNK/p38 MAPK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xiao-lu Wang ◽  
Liang Wang ◽  
Fo-lan Lin ◽  
Si-si Li ◽  
Ting-xuan Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Membrane ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Tunel Assay ◽  
Mapk Signaling Pathway ◽  
Mapk Activation ◽  
Urea Nitrogen

Copper/zinc superoxide dismutase (SOD1) can clear cisplatin- (CP-) induced excessive reactive oxygen species (ROS), but exogenous SOD1 cannot enter cells because of its low biomembrane permeability. Cell-penetrating peptides (CPPs) can rapidly cross plasma membranes. This study is aimed at identifying an efficient and stable CPP-SOD1 and investigating its effects on CP-induced nephrotoxicity. We recombined SOD1 with 14 different CPPs and purified them using an NTA-Ni2+ column. In in vitro experiments, CPPs-SOD1 cell membrane penetration ability and JNK/p38 MAPK signaling pathway were evaluated using Western blotting. ROS production, mitochondrial membrane potential (MMP), and cell apoptosis were determined using flow cytometry and immunofluorescence staining in VERO and HK-2 cells. For in vivo experiments, mice were administered PSF-SOD1 for 2 h before cotreatment with a single CP injection for an additional 4 days. Blood and kidney samples were collected for renal function assessment (creatinine, urea nitrogen, histopathology, TUNEL assay, and JNK/p38 MAPK signaling pathway). Compared with TAT-SOD1, we found that PSF-SOD1 is more efficient at crossing the cell membrane and is stable after transduction into cells. Pretreatment with PSF-SOD1 inhibited CP-induced apoptosis, ROS generation, and JNK/p38 MAPK activation and restored CP-induced MMP loss in VERO and HK-2 kidney cells. Treatment of mice with PSF-SOD1 inhibited CP-induced serum creatinine, blood urea nitrogen elevation, and JNK/p38 MAPK activation. H&E staining and TUNEL assay indicated that kidney tissue damage was alleviated following PSF-SOD1 pretreatment. Overall, PSF-SOD1 ameliorated CP-induced renal damage by partially reducing oxidative stress and cell apoptosis by regulating JNK/p38 MAPK signaling pathway and might be a better cytoprotective agent than TAT-SOD1.

scholarly journals Characterization of Apoptosis, Autophagy and Oxidative Stress in Pancreatic Islets Cells and Intestinal Epithelial Cells Isolated from Equine Metabolic Syndrome (EMS) Horses

2018 ◽  
Vol 19 (10) ◽  
pp. 3068
Author(s):  
Katarzyna Kornicka ◽  
Agnieszka Śmieszek ◽  
Jolanta Szłapka-Kosarzewska ◽  
Jennifer Irwin Houston ◽  
Michael Roecken ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Pancreatic Islets ◽  
Building Blocks ◽  
Protective Mechanism ◽  
Endocrine Disorders ◽  
Intestinal Epithelial ◽  
Epithelial Stem Cells ◽  
Equine Metabolic Syndrome

Endocrine disorders are becoming an increasing problem in both human and veterinary medicine. In recent years, more and more horses worldwide have been suffering from equine metabolic syndrome (EMS). This metabolic disorder is characterized by pathological obesity, hyperinsulinaemia, hyperglycaemia and insulin resistance. Although metabolic disorders, including diabetes, have been extensively studied, there are still no data on the molecular effects of EMS in horses. Thus, the aim of this study was to evaluate apoptosis, oxidative stress, autophagy and microRNA (miR) expression in multipotent intestinal epithelial stem cells (IECs) and pancreatic islets (PIs) isolated post mortem form healthy and EMS diagnosed horses. Our group was the first to describe how EMS affects IEC and PI aging and senescence. First, we evaluated isolation and culture protocol for these cells and subsequently established their metabolic status in vitro. Both IECs and PIs isolated from EMS horses were characterized by increased apoptosis and senescence. Moreover, they accumulated elevated levels of reactive oxygen species (ROS). Here we have observed that autophagy/mitophagy may be a protective mechanism which allows those cells to maintain their physiological function, clear protein aggregates and remove damaged organelles. Furthermore, it may play a crucial role in reducing endoplasmic reticulum (ER) stress. This protective mechanism may help to overcome the harmful effects of ROS and provide building blocks for protein and ATP synthesis.

scholarly journals Protective effects of alfalfa saponins on oxidative stress-induced apoptotic cells

2020 ◽  
Vol 11 (9) ◽  
pp. 8133-8140
Author(s):  
Yalei Cui ◽  
Boshuai Liu ◽  
Xiao Sun ◽  
Zidan Li ◽  
Yanyan Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Antioxidant System ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Apoptotic Cells ◽  
Protective Effects

Alfalfa saponins defend against oxidative stress by enhancing the antioxidant system and further inhibit cell apoptosis by activating the MAPK signaling pathway.

Fibronectin Type III Domain Containing 5 Alleviates the Inflammation and Apoptosis in Lipopolysaccharide- Induced Intestinal Epithelial Cells

2020 ◽  
Vol 10 (5) ◽  
pp. 669-675
Author(s):  
Junzhi Pan ◽  
Jie Zhang
Keyword(s):  
Oxidative Stress ◽  
Cell Apoptosis ◽  
Intestinal Injury ◽  
Intestinal Epithelial ◽  
Sod Activity ◽  
Fibronectin Type Iii ◽  
Fibronectin Type Iii Domain ◽  
Related Proteins ◽  
Fibronectin Type

Intestinal injury caused by sepsis has multiple effects on the pathophysiology and development of sepsis. In this study, we aimed to explore the role of FNDC5 in progression of sepsis-induced intestinal injury. The expression of FNDC5 in blood samples of patients with sepsis-induced intestinal injury and IEC-6 cells was measured by qRT-PCR assay. Cell viability and inflammatory cytokines were evaluated by CCK-8 and ELISA assay, respectively. Oxidative stress level was detected by DCFH-DA staining and corresponding kit. Tunel assay and western blot analysis were performed to assess cell apoptosis. FNDC5 expression in patients with sepsis-induced intestinal injury was significantly decreased. The stimulation of LPS reduced expression level of FNDC5 and inhibited cell growth in IEC-6 cells. Overexpression of FNDC5 suppressed the productions of TNF-a, IL-1 , IL-6 and MCP1, diminished the level of ROS and MPO while enhanced the SOD activity. Additionally, upregulation of FNDC5 ameliorated cell apoptosis and repressed the levels of apoptosis-related proteins. FNDC5 could play a crucial role in the inflammation, oxidative stress and apoptosis in sepsis-induced intestinal injury.

scholarly journals Naoxintong/PPARαSignaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Huimin Xu ◽  
Jianhua Jin ◽  
Lu Chen ◽  
Chunxiao Li ◽  
Qinggang Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Flow Cytometry ◽  
Chinese Medicine ◽  
Cardiovascular Diseases ◽  
Protective Effect ◽  
Cell Apoptosis ◽  
H9c2 Cell ◽  
Protective Mechanism ◽  
H9c2 Cells ◽  
Protein Levels

Naoxintong (NXT) is an empirical formula based on the principle of traditional Chinese medicine, which has been approved by China Food and Drug Administration (CFDA) and is widely used for treatment of patients with cerebrovascular and cardiovascular diseases in China. The aim of this study is to investigate the protective mechanism of NXT on H9c2 cells (cardiogenic cell line) in response to H2O2. MTT, Western blot, and flow cytometry (FCM) methods were used to identify the protective effect of NXT extract on H2O2-induced H9c2 cells. Here we found that NXT extract significantly increased H9c2 cell viability and reduced H2O2-induced cell apoptosis and autophagy. More importantly, NXT inhibited H2O2-induced H9c2 cell apoptosis and autophagy by increasing PPARαprotein levels. In contrast, silenced PPARαterminated NXT protective effect on H2O2-induced H9c2 cells. These findings suggest that NXT/PPARαsignaling suppressed H2O2-induced H9c2 cell apoptosis and autophagy.

scholarly journals l-Arginine Alleviates LPS-Induced Oxidative Stress and Apoptosis via Activating SIRT1-AKT-Nrf2 and SIRT1-FOXO3a Signaling Pathways in C2C12 Myotube Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1957
Author(s):  
Ye Zhao ◽  
Qin Jiang ◽  
Xuefei Zhang ◽  
Xiaoxiao Zhu ◽  
Xia Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Cell Apoptosis ◽  
Muscle Injury ◽  
Protective Mechanism ◽  
Nrf2 Signaling Pathway ◽  
Wide Range ◽  
Range Of Functions ◽  
Sirt1 Inhibitor ◽  
C2c12 Myotube

l-arginine (l-Arg) has been reported to possess a wide range of functions, including anti-inflammatory, anti-oxidative, and anti-apoptosis. However, the role of l-Arg in LPS-induced muscle injury and its potential protective mechanism has not been well elucidated. This study aimed to investigate the effects of l-Arg on the LPS-induced oxidative stress and apoptosis in differentiated C2C12 myotube cells. Our results demonstrated that myotube cells treated with 0.2 mg/mL LPS significantly decreased cell viability. l-Arg treatment significantly suppressed LPS induced ROS accumulation and cell apoptosis. Furthermore, l-Arg improved antioxidant-related enzymes’ activities; increased antioxidant ability via Akt-Nrf2 signaling pathway; maintained the mitochondrial membrane potential (MMP); and enhanced FOXO3a expression, leading to a decrease in the mitochondrial-associated apoptotic proteins. In addition, l-Arg exposure dramatically increased the mRNA and protein expressions of SIRT1. The cytoprotective effect of l-Arg was restricted by the SIRT1 inhibitor EX527, which led to an increase in ROS level, apoptosis rate, and decreased cell MMP. The results also demonstrated that EX527 treatment significantly eliminated the effect of l-Arg on LPS-induced oxidative damage and mitochondria-mediated cell apoptosis. Our findings revealed that l-Arg could be used as a potential nutraceutical in reducing muscle injury via regulating SIRT1-Akt-Nrf2 and SIRT1-FOXO3a-mitochondria apoptosis signaling pathways.

scholarly journals Alfalfa saponins inhibit oxidative stress-induced cell apoptosis through the MAPK signaling pathway

Redox Report ◽  
2021 ◽  
Vol 27 (1) ◽  
pp. 1-8
Author(s):  
Yalei Cui ◽  
Fen Li ◽  
Xiaoyan Zhu ◽  
Junying Xu ◽  
Abaidullah Muhammad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway

scholarly journals The Impact of Herbal Infusion Consumption on Oxidative Stress and Cancer: The Good, the Bad, the Misunderstood

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4207 ◽  
Author(s):  
Wamidh H. Talib ◽  
Israa A. AL-ataby ◽  
Asma Ismail Mahmod ◽  
Sajidah Jawarneh ◽  
Lina T. Al Kury ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Causal Link ◽  
Cancer Development ◽  
Protective Mechanism ◽  
Oxygen Species ◽  
Antioxidant Supplements ◽  
Herbal Infusions ◽  
The Impact ◽  
Antioxidant Effects ◽  
And Oxidative Stress

The release of reactive oxygen species (ROS) and oxidative stress is associated with the development of many ailments, including cardiovascular diseases, diabetes and cancer. The causal link between oxidative stress and cancer is well established and antioxidants are suggested as a protective mechanism against cancer development. Recently, an increase in the consumption of antioxidant supplements was observed globally. The main sources of these antioxidants include fruits, vegetables, and beverage. Herbal infusions are highly popular beverages consumed daily for different reasons. Studies showed the potent antioxidant effects of plants used in the preparation of some herbal infusions. Such herbal infusions represent an important source of antioxidants and can be used as a dietary protection against cancer. However, uncontrolled consumption of herbal infusions may cause toxicity and reduced antioxidant activity. In this review, eleven widely consumed herbal infusions were evaluated for their antioxidant capacities, anticancer potential and possible toxicity. These herbal infusions are highly popular and consumed as daily drinks in different countries. Studies discussed in this review will provide a solid ground for researchers to have better understanding of the use of herbal infusions to reduce oxidative stress and as protective supplements against cancer development.

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