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.

Albicanol antagonizes Cd-induced apoptosis through a NO/iNOS-regulated mitochondrial pathway in chicken liver cells

2021 ◽  
Author(s):  
Yalin Guan ◽  
Xia Zhao ◽  
Nuan Song ◽  
Yuan Cui ◽  
Ying Chang
Keyword(s):  
Free Radical ◽  
Mitochondrial Pathway ◽  
Liver Cells ◽  
Chicken Liver ◽  
Mitochondrial Apoptosis ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway ◽  
Induced Apoptosis

Albicanol can reduce the excessive production of the NO free radical induced by Cd, and then inhibits the mitochondrial apoptosis pathway.

Rituximab Sensitizes TRAIL-Resistant B-NHL Lines to Apoptosis by Both TRAIL and Fully Humanized Antibodies Targeting TRAIL-R1 (Mapatumumab) and TRAIL-R2 (Lexatumumab).

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2350-2350 ◽  
Author(s):  
Mario I. Vega ◽  
Sara Huerta-Yepez ◽  
Stavroula Baritaki ◽  
Melisa A. Martinez-Paniagua ◽  
Cesar R. Gonzalez-Bonilla ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Tumor Cells ◽  
Direct Role ◽  
Annual Meeting Abstract ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway ◽  
Fas L ◽  
Induced Apoptosis ◽  
Humanized Monoclonal Antibodies

Abstract Clinical trials are currently in progress to evaluate the therapeutic efficacy of recombinant human TRAIL and fully humanized monoclonal antibodies that target TRAIL-R1 (DR4, mapatumumab) and TRAIL-R2 (DR5, lexatumumab). Although these proteins are cytotoxic to sensitive tumor cells, many tumors are resistant and require a sensitization stimulus. We have reported that rituximab inhibits anti-apoptotic survival pathways such as NF-κB activity and sensitizes tumor cells to both chemotherapeutic drugs and Fas-L- induced apoptosis (Vega et al., J. Immunol175(4):2174–83, 2005). Sensitization to TRAIL is also regulated by NF-κB. Thus, we hypothesize that rituximab-induced inhibition of NF-κB also sensitizes B-NHL cells to TRAIL apoptosis. Treatment of Ramos, Daudi, 2F7 and Raji with rituximab sensitized the cells to TRAIL apoptosis in a concentration dependant feature. Sensitization to TRAIL by Rituximab involved the type II mitochondrial apoptosis pathway. Examination of the mechanism of rituximab sensitization to TRAIL revealed that inhibition of NF-κB was associated with inhibition of the DR5 transcription repressor Yin Yang 1 (YY1) and up regulation of DR5 (Vega et al., Blood 108(11):2387, ASH Annual Meeting Abstract 2006). There was no up regulation of DR4 by rituximab. The direct role of YY1 in the rituximab induced sensitization to TRAIL was corroborated by YY1siRNA. These findings suggested that one mechanism of Rituximab sensitization to TRAIL involved up regulation of DR5 expression. However, since TRAIL binds to both DR4 and DR5, the role of DR4 in rituximab induced sensitization to TRAIL needed further clarification. This was addressed by the use of the specific fully humanized monoclonal antibodies directed against DR4 (TRAIL-R1) (HGS-ETR1, mapatumumab) and DR5 (TRAIL-R2) (HGS-ETR2, lexatumumab) provided by Human Genome Sciences. Treatment of Ramos with rituximab sensitized the cells to both HGS-ETR1 and HGS-ETR2 induced apoptosis in a concentration dependant fashion. The sensitization by these antibodies was comparable to that achieved with TRAIL. These findings demonstrate that rituximab sensitizes B-NHL cells to both TRAIL and DR4/DR5 agonist-antibodies. The studies also suggest that, while the up regulation of DR5 expression by rituximab via inhibition of YY1 was critical for TRAIL apoptosis, up regulation of DR4 by rituximab was not required for sensitization with HGS-ETR1 monoclonal antibody. Further, these results suggest that rituximab may affect cell signaling induced by both DR4 and DR5. The molecular mechanism by which rituximab sensitizes B-NHL cells to TRAIL and both HGS-ETR1 and HGS-ETR2 will be presented.

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 Shen Shuai II Recipe attenuates apoptosis in 5/6th renal ablation/infarction rats by inhibiting p53 and mitochondrial pathway of apoptosis

2019 ◽  
Author(s):  
Meng Wang ◽  
Jing Yang ◽  
Liuyi Yang ◽  
Chen Wang
Keyword(s):  
Underlying Mechanism ◽  
Mitochondrial Pathway ◽  
Global Public Health ◽  
Sprague Dawley ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway ◽  
Mitochondrial Translocation ◽  
Renal Ablation ◽  
Losartan Group ◽  
Group 5

Abstract Background Chronic kidney disease (CKD) has become a serious challenge to global public health. Apoptosis is closely related to the evolution of CKD. In China, it has been noted that Chinese herbal medicine may be suitable for the treatment of CKD. Shen Shuai II Recipe (SSR) is a classic formula for the treatment of CKD in the clinic and proves the renprotective effects. However, the underlying mechanism remains unclear. The main purpose of this study was to investigate whether SSR could reduce apoptosis in 5/6 renal ablation/infarction (A/I) hypoxia model by regulating p53 and mitochondrial pathway of apoptosis.Methods 28 days after the 5/6 (A/I) surgery, Sprague-Dawley rats were randomly divided into four groups: sham group, 5/6 (A/I) group, 5/6 (A/I) + SSR group and 5/6 (A/I) +Losartan group (5/6 (A/I) +LOR). After 56 days of treatment, we mainly assessed the translocation of apoptotic factors in mitochondrial apoptosis pathway, the degree of mitochondrial dysfunction and the nuclear and mitochondrial translocation of p53. Furthermore, we detected the interaction of p53 with anti-apoptotic Bcl-xL and Bcl-2 proteins.Results SSR significantly inhibited the mitochondrial accumulation of pro-apoptotic protein Bax and Puma and release of cytochrome c from mitochondria to cytosol in the 5/6 (A/I) model. In addition, SSR improved the mitochondrial function and inhibited the nuclear and mitochondrial translocation of p53. SSR suppressed the p53 transactivation and the interaction of p53 with Bcl-xL and Bcl-2.Conclusions These results suggested that SSR could exert anti-apoptotic effects in the 5/6 (A/I) hypoxia model by inhibiting p53 transcriptional dependent and independent pro-apoptotic functions and the mitochondrial pathway of apoptosis.

scholarly journals UVB protective effects of Sargassum horneri through the regulation of Nrf2 mediated antioxidant mechanism

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eui Jeong Han ◽  
Seo-Young Kim ◽  
Hee-Jin Han ◽  
Hyun-Soo Kim ◽  
Kil-Nam Kim ◽  
...  
Keyword(s):  
Skin Barrier ◽  
Human Keratinocytes ◽  
Underlying Mechanism ◽  
Ultraviolet B ◽  
Sargassum Horneri ◽  
Cellular Damage ◽  
Protective Effects ◽  
Skin Damage ◽  
Antioxidant Mechanism ◽  
Induced Apoptosis

AbstractThe present study aimed to evaluate the protective effect of a methanol extract of Sargassum horneri (SHM), which contains 6-hydroxy-4,4,7a-trimethyl-5,6,7,7a-tetrahydrobenzofuran-2(4H)-one (HTT) and apo-9′-fucoxanthinone, against ultraviolet B (UVB)-induced cellular damage in human keratinocytes and its underlying mechanism. SHM significantly improved cell viability of UVB-exposed human keratinocytes by reducing the generation of intracellular reactive oxygen species (ROS). Moreover, SHM inhibited UVB exposure-induced apoptosis by reducing the formation of apoptotic bodies and the populations of the sub-G1 hypodiploid cells and the early apoptotic cells by modulating the expression of the anti- and pro-apoptotic molecules, Bcl-2 and Bax, respectively. Furthermore, SHM inhibited NF-κB p65 activation by inducing the activation of Nrf2/HO-1 signaling. The cytoprotective and antiapoptotic activities of SHM are abolished by the inhibition of HO-1 signaling. In further study, SHM restored the skin dryness and skin barrier disruption in UVB-exposed human keratinocytes. Based to these results, our study suggests that SHM protects the cells against UVB-induced cellular damages through the Nrf2/HO-1/NF-κB p65 signaling pathway and may be potentially useful for the prevention of UVB-induced skin damage.

Mechanism of cadmium induced apoptosis in human peripheral blood lymphocytes: The role of p53, Fas and Caspase-3

2013 ◽  
Vol 36 (3) ◽  
pp. 1033-1039 ◽  
Author(s):  
Abdullah H. Al-Assaf ◽  
Ali M. Alqahtani ◽  
Ali A. Alshatwi ◽  
Naveed A. Syed ◽  
Gowhar Shafi ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Caspase 3 ◽  
Human Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Blood Lymphocytes ◽  
Human Peripheral Blood Lymphocytes ◽  
Induced Apoptosis

scholarly journals Modulatory effect of Persea Americana oil against diethylnitrosamine-induced hepatotoxicity in rats: a proposed mechanism

2021 ◽  
Vol 45 (1) ◽  
Author(s):  
Omayma A. R. Abozaid ◽  
Lobna M. Anees ◽  
Gehan R. Abdel-Hamed
Keyword(s):  
Nadph Oxidase ◽  
Caspase 3 ◽  
Persea Americana ◽  
Gene Expressions ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway ◽  
Apoptotic Effect ◽  
Oxide Synthase ◽  
Parp 1 ◽  
Inducible Nitric Oxide

Abstract Background The purpose of this study was to investigate the effectiveness of Persea Americana (avocado) oil against diethylnitrosamine (DEN)-induced hepatotoxicity in rats. Methods For the induction of hepatotoxicity, DEN was administrated orally in a dose of 20 mg/kg B.wt for 6 successive weeks, and then the animals were gavaged with Persea Americana oil in a dose of 4 mL/kg b.wt. daily for another 6 weeks. Serum caspase-3 activity and poly (ADP-ribose) polymerase-1 (PARP-1) levels were estimated; in addition to gene expressions for NADPH oxidase, inducible nitric oxide synthase (iNOS), Bcl-2, and Bax were detected. Results The DEN-intoxicated group exhibited a remarkable increase in NADPH oxidase and iNOS expression combined with over-activation of PARP-1 and increased antiapoptotic Bcl-2 gene expression, whereas the expression of apoptotic biomarkers significantly decreased. On the other hand, treatment with Persea Americana oil significantly suppressed the elevated levels of hepatic enzymes and improved histopathological alterations in the liver. Furthermore, these groups displayed marked downregulation in NADPH oxidase and iNOS expressions. Persea Americana oil suppressed the expression of the antiapoptotic Bcl-2, activated the intrinsic mitochondrial apoptosis pathway through upregulation of pro-apoptotic Bax, and induced an obvious increase in caspase-3 activity. Moreover, Persea Americana oil administration markedly inhibited the activity of PARP-1. Conclusions This study indicated the promising potential of Persea Americana oil against DEN-induced hepatic injury through its anti-oxidative activity and pro-apoptotic effect via caspase activation and PARP-1 inhibition.

scholarly journals UFL1 Alleviates LPS-Induced Apoptosis by Regulating the NF-κB Signaling Pathway in Bovine Ovarian Granulosa Cells

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 260 ◽  
Author(s):  
Xinling Wang ◽  
Chengmin Li ◽  
Yiru Wang ◽  
Lian Li ◽  
Zhaoyu Han ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Granulosa Cells ◽  
Protein Concentration ◽  
Caspase 3 ◽  
Nuclear Factor Κb ◽  
Ovarian Granulosa Cells ◽  
Induced Apoptosis ◽  
Apoptosis Level ◽  
Lps Treatment

Ubiquitin-like modifier 1 ligating enzyme 1 (UFL1) is an E3 ligase of ubiquitin fold modifier 1 (UFM1), which can act together with its target protein to inhibit the apoptosis of cells. Lipopolysaccharides (LPS) can affect the ovarian health of female animals by affecting the apoptosis of ovarian granulosa cells. The physiological function of UFL1 on the apoptosis of bovine (ovarian) granulosa cells (bGCs) remains unclear; therefore, we focused on the modulating effect of UFL1 on the regulation of LPS-induced apoptosis in ovarian granulosa cells. Our study found that UFL1 was expressed in both the nucleus and cytoplasm of bGCs. The results here demonstrated that LPS caused a significant increase in the apoptosis level of bGCs in cows, and also dramatically increased the expression of UFL1. Furthermore, we found that UFL1 depletion caused a significant increase in apoptosis (increased the expression of BAX/BCL-2 and the activity of caspase-3). Conversely, the overexpression of UFL1 relieved the LPS-induced apoptosis. In order to assess whether the inhibition of bGCs apoptosis involved in the nuclear factor-κB (NF-κB) signaling pathway resulted from UFL1, we detected the expression of NF-κB p-p65. LPS treatment resulted in a significant upregulation in the protein concentration of NF-κB p-p65, and knockdown of UFL1 further increased the phosphorylation of NF-κB p65, while UFL1 overexpression significantly inhibited the expression of NF-κB p-p65. Collectively, UFL1 could suppress LPS-induced apoptosis in cow ovarian granulosa cells, likely via the NF-κB pathway. These results identify a novel role of UFL1 in the modulation of bGC apoptosis, which may be a potential signaling target to improve the reproductive health of dairy cows.

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