Molecular mechanisms involved in the protective effect of the chloroform extract of Selaginella lepidophylla (Hook. et Grev.) Spring in a lithiasic rat model

Urolithiasis ◽  
2013 ◽  
Vol 41 (3) ◽  
pp. 205-215 ◽  
Author(s):  
Estévez-Carmona María Mirian ◽  
Narvaéz-Morales Juanita ◽  
Barbier Olivier Christophe ◽  
Meléndez-Camargo María Estela
2020 ◽  
Vol 2020 ◽  
pp. 1-22
Author(s):  
Guoxia Zhu ◽  
Yongxiang Wu ◽  
Yang Qiu ◽  
Keyong Tian ◽  
Wenjuan Mi ◽  
...  

Sound conditioning (SC) is defined as “toughening” to lower levels of sound over time, which reduces a subsequent noise-induced threshold shift. Although the protective effect of SC in mammals is generally understood, the exact mechanisms involved have not yet been elucidated. To confirm the protective effect of SC against noise exposure (NE) and the stress-related signaling pathway of its rescue, we observed target molecule changes caused by SC of low frequency prior to NE as well as histology analysis in vivo and verified the suggested mechanisms in SGNs in vitro. Further, we investigated the potential role of Hsp70 and Bmi1 in SC by targeting SOD1 and SOD2 which are regulated by the FoxO1 signaling pathway based on mitochondrial function and reactive oxygen species (ROS) levels. Finally, we sought to identify the possible molecular mechanisms associated with the beneficial effects of SC against noise-induced trauma. Data from the rat model were evaluated by western blot, immunofluorescence, and RT-PCR. The results revealed that SC upregulated Hsp70, Bmi1, FoxO1, SOD1, and SOD2 expression in spiral ganglion neurons (SGNs). Moreover, the auditory brainstem responses (ABRs) and electron microscopy revealed that SC could protect against acute acoustic trauma (AAT) based on a significant reduction of hearing impairment and visible reduction in outer hair cell loss as well as ultrastructural changes in OHCs and SGNs. Collectively, these results suggested that the contribution of Bmi1 toward decreased sensitivity to noise-induced trauma following SC was triggered by Hsp70 induction and associated with enhancement of the antioxidant system and decreased mitochondrial superoxide accumulation. This contribution of Bmi1 was achieved by direct targeting of SOD1 and SOD2, which was regulated by FoxO1. Therefore, the Hsp70/Bmi1-FoxO1-SOD signaling pathway might contribute to the protective effect of SC against AAT in a rat model.


2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.


Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 677
Author(s):  
Cristina Serra-Castelló ◽  
Ilario Ferrocino ◽  
Anna Jofré ◽  
Luca Cocolin ◽  
Sara Bover-Cid ◽  
...  

Formulations with lactate as an antimicrobial and high-pressure processing (HPP) as a lethal treatment are combined strategies used to control L. monocytogenes in cooked meat products. Previous studies have shown that when HPP is applied in products with lactate, the inactivation of L. monocytogenes is lower than that without lactate. The purpose of the present work was to identify the molecular mechanisms underlying the piezo-protection effect of lactate. Two L. monocytogenes strains (CTC1034 and EGDe) were independently inoculated in a cooked ham model medium without and with 2.8% potassium lactate. Samples were pressurized at 400 MPa for 10 min at 10 °C. Samples were subjected to RNA extraction, and a shotgun transcriptome sequencing was performed. The short exposure of L. monocytogenes cells to lactate through its inoculation in a cooked ham model with lactate 1h before HPP promoted a shift in the pathogen’s central metabolism, favoring the metabolism of propanediol and ethanolamine together with the synthesis of the B12 cofactor. Moreover, the results suggest an activated methyl cycle that would promote modifications in membrane properties resulting in an enhanced resistance of the pathogen to HPP. This study provides insights on the mechanisms developed by L. monocytogenes in response to lactate and/or HPP and sheds light on the understanding of the piezo-protective effect of lactate.


RSC Advances ◽  
2017 ◽  
Vol 7 (63) ◽  
pp. 39929-39939 ◽  
Author(s):  
Jing Li ◽  
Wei Gao ◽  
Jining Gao ◽  
Hong Li ◽  
Xiang Zhang ◽  
...  

A 1H NMR based metabolomics approach combined with biochemical assay and histopathological inspection has been employed to study the protective effect of PEFF against asthma on a rat model.


2017 ◽  
Vol 16 (6) ◽  
pp. 1299 ◽  
Author(s):  
Shan Jing ◽  
Piaopiao Ying ◽  
Xiaohua Hu ◽  
Ze Yu ◽  
Jianwei Sun ◽  
...  

2019 ◽  
Author(s):  
Maryam Sarbishegi ◽  
Hamidreza Mahmoudzadeh-sagheb ◽  
Zahra Heidari ◽  
Farzaneh Baharvand

Abstract- Several studies point to an important role of neuroinflammation in Parkinson's disease (PD). Cognitive and memory impairments have been known in the early stages of PD. In the present study, we examined the effects of celecoxib (CLX), a selective inhibitor of cyclooxygenase-2 (COX-2), on hippocampus cell loss, passive avoidance memory and antioxidant status in a rat model of PD. We used the subcutaneous injection of 2.5 mg/kg/48h rotenone (ROT) for 4 weeks for induction of PD in a male Wistar rat. Animals were randomized to 4 groups (n=12): Control, sham, PD and PD+CLX group that receive celecoxib (20 mg/kg/day) for 4 weeks. Passive avoidance memory evaluated. We also determined the protective effect of CLX on a number of CA1 neurons in Nissl and TUNEL staining. Total antioxidant capacity (TAC) and malondialdehyde (MDA) a marker of lipid peroxidation in hippocampus assessed. Our findings indicated administration of CLX increase the passive avoidance memory (P<0.05), and by a decrease in apoptosis caused an increase in viable pyramidal neurons in CA1 hippocampus (P<0.01). On the other hand, CLX markedly reduced MDA level and increased TAC in the hippocampus of the PD model animal (P<0.05). It seems CLX with anti-inflammatory and antiapoptotic effect could prevent neurons loss and memory impairment which induced in PD.


2021 ◽  
Vol 58 (4) ◽  
pp. 241-248
Author(s):  
Fatma Atalay ◽  
◽  
Arzu Tatar ◽  
Busra Dincer ◽  
Betul Gundogdu ◽  
...  
Keyword(s):  

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