scholarly journals Compound Ammonium Glycyrrhizin Protects Hepatocytes from Injury Induced by Lipopolysaccharide/Florfenicol through a Mitochondrial Pathway

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2378 ◽  
Author(s):  
Wenyang Li ◽  
Ying Li ◽  
Xiangyuan Jiang ◽  
Xiaohui Li ◽  
Zugong Yu
Keyword(s):  
Liver Injury ◽  
Underlying Mechanism ◽  
Mitochondrial Pathway ◽  
Protective Role ◽  
Mitochondrial Damage ◽  
Apoptosis Pathway ◽  
Gene Level ◽  
Vitro Model

Florfenicol (FFC), a widely used drug for chicken diseases, can aggravate lipopolysaccharide (LPS) damage to the liver. For this condition, natural or synthetic products displaying strong antioxidant capacity are expected to prevent LPS/FFC from inducing liver injury, so in our study, the compound ammonium glycyrrhizin (CAG) is used as the protective drug to decrease the injury to liver. The research aims to illustrate the underlying mechanism of combining LPS with FFC-induced liver injury and the protective role of CAG by using primary chicken hepatocytes as an in vitro model. The results show that LPS/FFC induced cell apoptosis and CAG protected hepatocytes from injury. The permeability of the cell membrane is elevated by LPS/FFC, leading to the efflux of enzymes (ALT, AST). Flow cytometry analysis indicates that LPS/FFC treatment increased the apoptosis rate significantly. Furthermore, with the up-regulation of apoptosis genes bax, cytochrome c and the down-regulation of bcl-2, caspase-3 and caspase-9 are activated at the gene level. LPS/FFC-induced mitochondrial damage is accompanied by a significant decrease in mitochondrial membrane potential (MMP) and severe mitochondrial damage. However, CAG improves the situation for the purpose of protecting the liver. In conclusion, it is speculated that LPS/FFC induces severe liver injury through apoptosis and the CAG protects hepatocytes from injury via the mitochondria-mediated apoptosis pathway.

scholarly journals Lycium barbarumPolysaccharides Protect Rat Corneal Epithelial Cells against Ultraviolet B-Induced Apoptosis by Attenuating the Mitochondrial Pathway and Inhibiting JNK Phosphorylation

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Shaobo Du ◽  
Biao Han ◽  
Kang Li ◽  
Xuan Zhang ◽  
Xueli Sha ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Underlying Mechanism ◽  
Mitochondrial Pathway ◽  
Ultraviolet B ◽  
Lycium Barbarum ◽  
Apoptosis Pathway ◽  
Corneal Epithelial ◽  
Mitochondrial Apoptosis Pathway ◽  
Induced Apoptosis

Lycium barbarumpolysaccharides (LBPs) have been shown to play a key role in protecting the eyes by reducing the apoptosis induced by certain types of damage. However, it is not known whether LBPs can protect damaged corneal cells from apoptosis. Moreover, no reports have focused on the role of LBPs in guarding against ultraviolet B- (UVB-) induced apoptosis. The present study aimed to investigate the protective effect and underlying mechanism of LBPs against UVB-induced apoptosis in rat corneal epithelial (RCE) cells. The results showed that LBPs significantly prevented the loss of cell viability and inhibited cell apoptosis induced by UVB in RCE cells. LBPs also inhibited UVB-induced loss of mitochondrial membrane potential, downregulation ofBcl-2, and upregulation ofBaxand caspase-3. Finally, LBPs attenuated the phosphorylation of c-Jun NH2-terminal kinase (JNK) triggered by UVB. In summary, LBPs protect RCE cells against UVB-induced damage and apoptosis, and the underlying mechanism involves the attenuation of the mitochondrial apoptosis pathway and the inhibition of JNK phosphorylation.

scholarly journals Bornlisy Attenuates Colitis-Associated Colorectal Cancer via Inhibiting GPR43-Mediated Glycolysis

2021 ◽  
Vol 8 ◽  
Author(s):  
Xia Lu ◽  
Shuping Qiao ◽  
Chen Peng ◽  
Wenyue Yan ◽  
Zhen Xu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Antitumor Effect ◽  
Intervention Strategy ◽  
Underlying Mechanism ◽  
Protective Role ◽  
Erk Pathway ◽  
Proliferation And Metastasis

There is evidence that probiotics have a broad antitumor effect in colorectal cancer (CRC). However, the mechanism remains obscure. Here, we investigated the effect of Bornlisy (BO)-cocktails of three probiotics on colitis-associated colon cancer (CAC) and the underlying mechanism. The treatment of CAC mice with BO resulted in decreased tumor loads as compared with their counterparts. BO also inhibited the proliferation and metastasis of CRC cells in vitro. Furthermore, BO inhibited cell proliferation through downregulating glycolysis. Activating glycolysis reversed the protective role of BO in the CAC mice. Mechanically, BO administration promoted the activation of GPR43, followed by its downstream PLC-PKC-ERK pathway, which led to decreased glucose metabolism. These results suggest that BO may provide an intervention strategy for CRC therapy, while GPR43 is a potential targeting receptor during the BO treatment.

Genistein Suppresses the Isoproterenol-Treated H9c2 Cardiomyoblast Cell Apoptosis Associated with P-38, Erk1/2, JNK, and NFκB Signaling Protein Activation

2013 ◽  
Vol 41 (05) ◽  
pp. 1125-1136 ◽  
Author(s):  
Wei-Syun Hu ◽  
Yueh-Min Lin ◽  
Tsung-Jung Ho ◽  
Ray-Jade Chen ◽  
Yi-Hui Li ◽  
...  
Keyword(s):  
Menopausal Status ◽  
Image Data ◽  
Protective Role ◽  
Protein Activation ◽  
Receptor Modulator ◽  
Cellular Apoptosis ◽  
Cardio Protection ◽  
Vitro Model

Heart disease (HD) is associated with estrogen and therefore gender and menopausal status. In addition, clinical evidence shows that increased serum norepinephrine is found in patients with HD. Therefore, this study aimed to investigate the cardio-protective effect of genistein, a selective estrogen receptor modulator (SERM) from soy bean extract, in H9c2 cardiomyoblast cells treated with isoproterenol (ISO), a norepinephrine analog. In this in vitro model, image data and results from western blotting shown that ISO treatment was capable of inducing cellular apoptosis, especially the mitochondrial dependent pathway. Treatment of genistein could suppress the expression of mitochondrial pro-apoptotic proteins including Bad, caspase-8, caspase-9, and caspase-3 in H9c2 treated with ISO. By contrast, several survival proteins were expressed in H9c2 treated with genistein, such as phosphor (p)-Akt, p-Bad, and p-Erk1/2. Furthermore, we confirmed that the protective role of genistein was partially mediated through the expression of Erk1/2, Akt, and NF κ B proteins by adding several pathway inhibitors. These in vitro data suggest that genistein may be a safe and natural SERM alternative to hormone therapy in cardio-protection.

scholarly journals Protective Role of AMP-Activated Protein Kinase-Evoked Autophagy on an In Vitro Model of Ischemia/Reperfusion-Induced Renal Tubular Cell Injury

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79814 ◽  
Author(s):  
Li-Ting Wang ◽  
Bo-Lin Chen ◽  
Cheng-Tien Wu ◽  
Kuo-How Huang ◽  
Chih-Kang Chiang ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Renal Tubular Cell ◽  
Vitro Model ◽  
Renal Tubular ◽  
Amp Activated Protein Kinase

scholarly journals TGR5 deficiency aggravates hepatic ischemic/reperfusion injury via inhibiting SIRT3/FOXO3/HIF-1ɑ pathway

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Qi Wang ◽  
Song Wei ◽  
Lei Li ◽  
Jiannan Qiu ◽  
Shun Zhou ◽  
...  
Keyword(s):  
Liver Injury ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
In Vitro Experiments ◽  
Proinflammatory Response ◽  
Forkhead Box ◽  
Membrane Bound ◽  
G Protein Coupled

Abstract Ischemia/reperfusion (I/R) injury is responsible for liver injury during hepatic resection and liver transplantation. The plasma membrane-bound G protein-coupled bile acid receptor (TGR5) could regulate immune response in multiple liver diseases. Nevertheless, the underlying role of TGR5 in hepatic I/R injury remains largely unknown. This study aimed to investigate the potential mechanism of TGR5 in hepatic I/R injury. Wild-type (WT) and TGR5 knockout (TGR5KO) mice were used to perform hepatic I/R, and macrophages were isolated from mice for in vitro experiments. The results demonstrated that knockout of TGR5 in mice significantly exacerbated liver injury and inflammatory response. TGR5KO mice infused with WT macrophages showed relieved liver injury. Further study revealed that TGR5 knockout inhibited sirtuin 3 (SIRT3) and forkhead box O3 (FOXO3) expression. In vitro experiments indicated that SIRT3 inhibited acetylation, ubiquitination and degradation of FOXO3. FOXO3 inhibited HIF-1α transcription by binding to its promoter. TGR5 knockout inhibited SIRT3 expression, thus promoted the acetylation, ubiquitination, and degradation of FOXO3, which resulted in increased HIF-1α transcription and macrophages proinflammatory response. Collectively, TGR5 plays a critical protective role in hepatic I/R injury. FOXO3 deacetylation mediated by SIRT3 can attenuate hepatic I/R injury. TGR5 deficiency aggravates hepatic I/R injury via inhibiting SIRT3/FOXO3/HIF-1α pathway.

scholarly journals Extracellular vesicles shuttle protective messages against heat stress in bovine granulosa cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Samuel Gebremedhn ◽  
Ahmed Gad ◽  
Hoda Samir Aglan ◽  
Jozef Laurincik ◽  
Radek Prochazka ◽  
...  
Keyword(s):  
Heat Stress ◽  
Extracellular Vesicles ◽  
Granulosa Cells ◽  
Beef Cows ◽  
Protective Role ◽  
Bioactive Molecules ◽  
Follicular Cells ◽  
Vitro Model

Abstract Elevated summer temperature is reported to be the leading cause of stress in dairy and beef cows, which negatively affects various reproductive functions. Follicular cells respond to heat stress (HS) by activating the expression of heat shock family proteins (HSPs) and other antioxidants. HS is reported to negatively affect the bi-directional communication between the follicular cells and the oocyte, which is partly mediated by follicular fluid extracellular vesicles (EVs) released from surrounding cells. As carriers of bioactive molecules (DNA, RNA, protein, and lipids), the involvement of EVs in mediating the stress response in follicular cells is not fully understood. Here we used an in vitro model to decipher the cellular and EV-coupled miRNAs of bovine granulosa cells in response to HS. Moreover, the protective role of stress-related EVs against subsequent HS was assessed. For this, bovine granulosa cells from smaller follicles were cultured in vitro and after sub-confluency, cells were either kept at 37 °C or subjected to HS (42 °C). Results showed that granulosa cells exposed to HS increased the accumulation of ROS, total oxidized protein, apoptosis, and the expression of HSPs and antioxidants, while the viability of cells was reduced. Moreover, 14 and 6 miRNAs were differentially expressed in heat-stressed granulosa cells and the corresponding EVs, respectively. Supplementation of stress-related EVs in cultured granulosa cells has induced adaptive response to subsequent HS. However, this potential was not pronounced when the cells were kept under 37 °C. Taking together, EVs generated from granulosa cells exposed to HS has the potential to shuttle bioactive molecules to recipient cells and make them robust to subsequent HS.

Nano-Curcumin Regulates p53 Phosphorylation and PAI-1 Expression during Bleomycin Induced Injury in Alveolar Basal Epithelial Cells

2020 ◽  
Vol 16 (1) ◽  
pp. 85-89
Author(s):  
Mahesh M. Gouda ◽  
Ashwini Prabhu ◽  
Varsha Reddy S.V. ◽  
Rafa Jahan ◽  
Yashodhar P. Bhandary
Keyword(s):  
Epithelial Cells ◽  
Lung Injury ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Plasminogen Activator Inhibitor ◽  
Underlying Mechanism ◽  
Protective Role ◽  
Alveolar Epithelial Cells ◽  
Cellular Damage

Background: Bleomycin (BLM) is known to cause DNA damage in the Alveolar Epithelial Cells (AECs). It is reported that BLM is involved in the up-regulation of inflammatory molecules such as neutrophils, macrophages, chemokines and cytokines. The complex underlying mechanism for inflammation mediated progression of lung injury is still unclear. This investigation was designed to understand the molecular mechanisms associated with p53 mediated modulation of Plasminogen Activator Inhibitor-I (PAI-I) expression and its regulation by nano-curcumin formulation. Methods: A549 cells were treated with BLM to cause the cellular damage in vitro and commercially available nano-curcumin formulation was used as an intervention. Cytotoxic effect of nano-curcumin was analyzed using Methyl Thiazolyl Tetrazolium (MTT) assay. Protein expressions were analyzed using western blot to evaluate the p53 mediated changes in PAI-I expression. Results: Nano-curcumin showed cytotoxicity up to 88.5 % at a concentration of 20 μg/ml after 48 h of treatment. BLM exposure to the cells activated the phosphorylation of p53, which in turn increased PAII expression. Nano-curcumin treatment showed a protective role against phosphorylation of p53 and PAI-I expression, which in turn regulated the fibro-proliferative phase of injury induced by bleomycin. Conclusion: Nano-curcumin could be used as an effective intervention to regulate the severity of lung injury, apoptosis of AECs and fibro-proliferation during pulmonary injury.

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