Protective effects of apigenin on LPS-induced endometritis via activating Nrf2 signaling pathway

2018 ◽  
Vol 123 ◽  
pp. 139-143 ◽  
Author(s):  
Pei-Yue Jiang ◽  
Xiao-Jun Zhu ◽  
Yi-Na Zhang ◽  
Fei-Fei Zhou ◽  
Xiao-Fu Yang
Keyword(s):  
Signaling Pathway ◽  
Protective Effects ◽  
Nrf2 Signaling Pathway

scholarly journals Protective Effects of 6,7,4′-Trihydroxyflavanone on Hypoxia-Induced Neurotoxicity by Enhancement of HO-1 through Nrf2 Signaling Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 341 ◽  
Author(s):  
Hyun-Su Lee ◽  
Gil-Saeng Jeong
Keyword(s):  
Signaling Pathway ◽  
Neurodegenerative Disorders ◽  
Nuclear Translocation ◽  
Protoporphyrin Ix ◽  
Protective Role ◽  
Osteoclast Formation ◽  
Protective Effects ◽  
Protein Levels ◽  
Nrf2 Signaling Pathway ◽  
Pre Treatment

Since hypoxia-induced neurotoxicity is one of the major causes of neurodegenerative disorders, including the Alzheimer’s disease, continuous efforts to find a novel antioxidant from natural products are required for public health. 6,7,4′-trihydroxyflavanone (THF), isolated from Dalbergia odorifera, has been shown to inhibit osteoclast formation and have an antibacterial activity. However, no evidence has reported whether THF has a protective role against hypoxia-induced neurotoxicity. In this study, we found that THF is not cytotoxic, but pre-treatment with THF has a cytoprotective effect on CoCl2-induced hypoxia by restoring the expression of anti-apoptotic proteins in SH-SY5y cells. In addition, pre-treatment with THF suppressed CoCl2-induced hypoxia-related genes including HIF1α, p53, VEGF, and GLUT1 at the mRNA and protein levels. Pre-treatment with THF also attenuated the oxidative stress occurred by CoCl2-induced hypoxia by preserving antioxidant proteins, including SOD and CAT. We revealed that treatment with THF promotes HO-1 expression through Nrf2 nuclear translocation. An inhibitor assay using tin protoporphyrin IX (SnPP) confirmed that the enhancement of HO-1 by pre-treatment with THF protects SH-SY5y cells from CoCl2-induced neurotoxicity under hypoxic conditions. Our results demonstrate the advantageous effects of THF against hypoxia-induced neurotoxicity through the HO-1/Nrf2 signaling pathway and provide a therapeutic insight for neurodegenerative disorders.

Astaxanthin and Nrf2 signaling pathway: a novel target for new therapeutic approaches

2021 ◽  
Vol 21 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Zahra Ahmadi ◽  
Habib Yaribeygi ◽  
Thozhukat Sathyapalan ◽  
Amirhossein Sahebkar
Keyword(s):  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Nuclear Translocation ◽  
Haematococcus Pluvialis ◽  
Primary Source ◽  
Redox Balance ◽  
Protective Effects ◽  
Beneficial Effects ◽  
New Therapeutic Approaches ◽  
Nrf2 Signaling Pathway

: Astaxanthin (AST) is a naturally occurring compound isolated from various sources such as fungi, plants, salmon, and crab. However, Haematococcus Pluvialis, a green alga, is the primary source of this beta carotenoid compound. AST has several favourable biological and pharmacological activities such as antioxidant, anti-inflammatory, anti-tumor, anti-diabetes, hepatoprotective and neuroprotective. Nevertheless, the exact molecular mechanisms of these protective effects of AST are unclear yet. The Nrf2 signaling pathway is one of the critical candidate signaling pathways that may be involved in these beneficial effects of AST. This signaling pathway is responsible for maintaining the redox balance in the physiologic state. Upon nuclear translocation, Nrf2 signaling activates antioxidant enzymes to reduce oxidative stress and protect cells against damage. In the current study, we have reviewed the effects of AST on the Nrf2 signaling pathway, which could potentially be developed as a novel therapeutic approach for the management of various diseases.

scholarly journals Protective Effects of Rice Peptide Oryza Peptide-P60 against Oxidative Injury through Activation of Nrf2 Signaling Pathway In Vitro and In Vivo

ACS Omega ◽  
2020 ◽  
Vol 5 (22) ◽  
pp. 13096-13107
Author(s):  
Chie Moritani ◽  
Kayoko Kawakami ◽  
Hiroshi Shimoda ◽  
Tadashi Hatanaka ◽  
Etsuko Suzaki ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Oxidative Injury ◽  
Protective Effects ◽  
Nrf2 Signaling Pathway

scholarly journals Effects of chitooligosaccharide-zinc on mice ovarian function in premature ovarian failure via regulating the sestrin2/nrf2 signaling pathway

2020 ◽  
Author(s):  
Jia Li ◽  
Yuhang Chen ◽  
Jiayu Xu ◽  
Jiangying Liu ◽  
Jiacheng Fu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ovarian Function ◽  
Treated Group ◽  
Control Group ◽  
Chitosan Oligosaccharide ◽  
Protective Effects ◽  
Developmental Defects ◽  
Adult Mice ◽  
Nrf2 Signaling Pathway ◽  
Significant Difference

Abstract BackgroundThe chitosan oligosaccharide-zinc (COS·Zn) is also a powerful antioxidant and anti-aging scavenger, whose anti-oxidative ability immensely exceeds that of vitamin C. Therefore, this study aimed to investigate the protective effects and potential mechanism by which COS·Zn improves ovarian function and delays aging in POF.MethodsThe female KM adult mice and POF mice were divided into treated and prevention groups; these were prophylactically or therapeutically administered COS·Zn (150mg/kg·d, 300mg/kg·d) for 21 days, respectively. ResultsThe number of antral follicles in COS·Zn-treated groups was lower in the treated and prevention groups than that in the control group, respectively. Obviously, the ovarian index, the level of FSH and LH all increased notably during the 300 mg/kg·d treated group and the prevention group compared with cy/bus groups. The expression of MVH, OCT4 and PCNA in the 300 mg/kg·d treated groups and MVH in the prevention groups were remarkably increased compared with the CY/BUS group. Meanwhile, the protein levels of P53 and P16 were markedly down-regulated in the treated groups and prevention groups compared with CY/BUS, except for the expression of P53 in the prevention groups. Furthermore, the Sestrin2 (SESN2) and SOD2 proteins were significantly higher in the 150 mg/kg·d treated group compared with the CY/BUS group, but the 300 mg/kg·d and CY/BUS group showed no significant difference in the level of SESN2. Similarly, the NRF2 and SESN2 proteins were up-regulated in the prevention groups, and the change in SOD2 was not significant. The results revealed increased GSH levels in the 150 mg/kg·d and 300 mg/kg·d treated groups compared with CY/BUS group, and the same trend was also shown in the prevention groups.1Conclusion COS·Zn improves ovarian and follicular developmental defects caused by regulating the sestrin2-nrf2 signaling pathway, and these results suggest a novel product that is effective a POF prevention and treatment drug.

scholarly journals Luteolin Alleviates AflatoxinB1-Induced Apoptosis and Oxidative Stress in the Liver of Mice through Activation of Nrf2 Signaling Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1268
Author(s):  
Shahid Ali Rajput ◽  
Aftab Shaukat ◽  
Kuntan Wu ◽  
Imran Rashid Rajput ◽  
Dost Muhammad Baloch ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Signaling Pathway ◽  
Aflatoxin B1 ◽  
Physiological Saline ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Protein Levels ◽  
Nrf2 Signaling Pathway ◽  
Induced Apoptosis

Aflatoxin B1 (AFB1), a threatening mycotoxin, usually provokes oxidative stress and causes hepatotoxicity in animals and humans. Luteolin (LUTN), well-known as an active phytochemical agent, acts as a strong antioxidant. This research was designed to investigate whether LUTN exerts protective effects against AFB1-induced hepatotoxicity and explore the possible molecular mechanism in mice. A total of forty-eight mice were randomly allocated following four treatment groups (n = 12): Group 1, physiological saline (CON). Group 2, treated with 0.75 mg/kg BW aflatoxin B1 (AFB1). Group 3, treated with 50 mg/kg BW luteolin (LUTN), and Group 4, treated with 0.75 mg/kg BW aflatoxin B1 + 50 mg/kg BW luteolin (AFB1 + LUTN). Our findings revealed that LUTN treatment significantly alleviated growth retardation and rescued liver injury by relieving the pathological and serum biochemical alterations (ALT, AST, ALP, and GGT) under AFB1 exposure. LUTN ameliorated AFB1-induced oxidative stress by scavenging ROS and MDA accumulation and boosting the capacity of the antioxidant enzyme (CAT, T-SOD, GSH-Px and T-AOC). Moreover, LUTN treatment considerably attenuates the AFB1-induced apoptosis in mouse liver, as demonstrated by declined apoptotic cells percentage, decreased Bax, Cyt-c, caspase-3 and caspase-9 transcription and protein with increased Bcl-2 expression. Notably, administration of LUTN up-regulated the Nrf2 and its associated downstream molecules (HO-1, NQO1, GCLC, SOD1) at mRNA and protein levels under AFB1 exposure. Our results indicated that LUTN effectively alleviated AFB1-induced liver injury, and the underlying mechanisms were associated with the activation of the Nrf2 signaling pathway. Taken together, LUTN may serve as a potential mitigator against AFB1-induced liver injury and could be helpful for the development of novel treatment to combat liver diseases in humans and/or animals.

scholarly journals Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 121 ◽  
Author(s):  
Lina Qi ◽  
Jingle Jiang ◽  
Jingfei Zhang ◽  
Lili Zhang ◽  
Tian Wang
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Protective Effects ◽  
Human Trophoblast ◽  
Nrf2 Signaling Pathway ◽  
Antioxidant Proteins ◽  
Pre Treatment ◽  
Induced Apoptosis ◽  
Excessive Accumulation

Pregnancy complications are associated with oxidative stress induced by accumulation of trophoblastic ROS in the placenta. We employed the human trophoblast HTR8/SVneo cell line to determine the effect of curcumin pre-treatment on H2O2-induced oxidative damage in HTR8/Sveo cells. Cells were pretreated with 2.5 or 5 μM curcumin for 24 h, and then incubated with 400 μM H2O2 for another 24 h. The results showed that H2O2 decreased the cell viability and induced excessive accumulation of reactive oxygen species (ROS) in HTR8/Sveo cells. Curcumin pre-treatment effectively protected HTR8/SVneo cells against oxidative stress-induced apoptosis via increasing Bcl-2/Bax ratio and decreasing the protein expression level of cleaved-caspase 3. Moreover, curcumin pre-treatment alleviated the excessive oxidative stress by enhancing the activity of antioxidative enzymes. The antioxidant effect of curcumin was achieved by activating Nrf2 and its downstream antioxidant proteins. In addition, knockdown of Nrf2 by Nrf2-siRNA transfection abolished the protective effects of curcumin on HTR8/SVneo cells against oxidative damage. Taken together, our results show that curcumin could protect HTR8/SVneo cells from H2O2-induced oxidative stress by activating Nrf2 signaling pathway.

scholarly journals Activation of AdipoR1 with rCTRP9 Preserves BBB Integrity through the APPL1/AMPK/Nrf2 Signaling Pathway in ICH Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Wei Zhao ◽  
Fanping Kong ◽  
Xiu Gong ◽  
Zaiyu Guo ◽  
Lianhua Zhao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Neuroprotective Effect ◽  
Neurological Impairment ◽  
Cerebrovascular Diseases ◽  
Neurological Deficits ◽  
Protective Effects ◽  
Nrf2 Signaling Pathway ◽  
Key Factor ◽  
Bbb Permeability ◽  
The Right

Background. The disruption of the blood brain barrier (BBB) is the key factor leading to neurological impairment after intracerebral hemorrhage (ICH) injury. Adiponectin receptor 1 (AdipoR1) has an important effect contributing to the integrity of BBB. As a homologue of adiponectin, recombinant C1q/TNF-related protein 9 (rCTRP9) has neuroprotective effect in cerebrovascular diseases. The aim of this study was to investigate the protective effect of AdipoR1 activation with rCTRP9 on BBB integrity after ICH injury and the potential mechanisms. Methods. 177 male mice were subjected in this study. ICH was induced by injecting collagenase into the right basal ganglia. rCTRP9 was treated intranasally at 1 hour after ICH. Selective siRNA was administered prior to ICH. Western blot, immunofluorescence staining, neurobehavioral tests, and BBB permeability were evaluated. Results. ICH increased the expression of endogenous AdipoR1 and CTRP9. Administration of rCTRP9 ameliorated neurological deficits and reduced the BBB permeability at 24 hours in ICH mice. Furthermore, rCTRP9 promoted the expression of AdipoR1, APPL1, p-AMPK, Nrf2, and tight junctional proteins. The intervention of specific siRNA of AdipoR1, APPL1, and p-AMPK reversed the protective effects of rCTRP9. Conclusions. Activation of AdipoR1 with rCTRP9 improved neurological functions and preserved BBB integrity through the APPL1/AMPK/Nrf2 signaling pathway in ICH mice. Therefore, CTRP9 could serve as a promising therapeutic method to alleviate BBB injury following ICH in patients.

scholarly journals Leonurine alleviates ferroptosis in cisplatin-induced acute kidney injury by activating the Nrf2 signaling pathway

2021 ◽  
Author(s):  
Jianqiang HU ◽  
Wenjing Gu ◽  
Ning Ma ◽  
Xiaoye Fan ◽  
Xinxin Ci
Keyword(s):  
Lipid Peroxidation ◽  
Acute Kidney Injury ◽  
Signaling Pathway ◽  
Lipid Peroxide ◽  
Kidney Injury ◽  
Iron Accumulation ◽  
Protective Effects ◽  
Nrf2 Signaling Pathway

Background and purpose: Increasing evidence suggests that ferroptosis plays a key role in the pathophysiology of acute kidney injury induced by cisplatin. The Nrf2 signaling pathway regulates oxidative stress and lipid peroxidation and positively regulates cisplatin-induced AKI (CI-AKI). However, Nrf2 and its activator leonurine on ferroptosis after CI-AKI remain unclear. Experimental Approach: The anti-ferroptotic effects of Nrf2 and its activator leonurine were assessed using a mouse model of cisplatin-induced AKI. In vitro, the potential effects of leonurine on erastin- and RSL3-induced HK-2 human PTEC ferroptosis were examined. Key Results: As expected, Nrf2 deletion induced ferroptosis-related protein expression and iron accumulation in vivo, further aggravating CI-AKI. The Nrf2 activator leonurine prevented iron accumulation and lipid peroxidation and inhibited ferroptosis in vitro, while these effects were abolished in siNrf2-treated cells. Moreover, leonurine potently ameliorated cisplatin-induced renal damage, as indicated by the assessment of SCr, BUN, KIM-1, and NGAL. Importantly, leonurine activated the Nrf2 antioxidative signaling pathway and prohibited changes in ferroptosis-related morphological and biochemical indicators, such as the MDA level, SOD and GSH depletion and GPX4 and xCT downregulation, in CI-AKI. Moreover, Nrf2 KO mice were more susceptible to ferroptosis after CI-AKI than control mice, and the protective effects of leonurine on AKI and ferroptosis were largely abolished in Nrf2 KO mice. Conclusion and Implications: These data suggest that the renal protective effects of Nrf2 and its activator leonurine on CI-AKI are achieved at least partially by inhibiting lipid peroxide-mediated ferroptosis and highlight the potential of leonurine as a CI-AKI treatment.

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