scholarly journals An Antioxidant Extract of the Insectivorous Plant Drosera burmannii Vahl. Alleviates Iron-Induced Oxidative Stress and Hepatic Injury in Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0128221 ◽  
Author(s):  
Nikhil Baban Ghate ◽  
Dipankar Chaudhuri ◽  
Abhishek Das ◽  
Sourav Panja ◽  
Nripendranath Mandal
2017 ◽  
Vol 13 (5) ◽  
pp. 1820-1826 ◽  
Author(s):  
Jinyan Zhao ◽  
Haixia Hu ◽  
Yun Wan ◽  
Yuchen Zhang ◽  
Liangpu Zheng ◽  
...  

Nanomedicine ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. 1423-1434 ◽  
Author(s):  
Ritesh K Shukla ◽  
Ashutosh Kumar ◽  
Naga Veera Srikanth Vallabani ◽  
Alok K Pandey ◽  
Alok Dhawan

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Yang Feng ◽  
Ruixia Cui ◽  
Zeyu Li ◽  
Xia Zhang ◽  
Yifan Jia ◽  
...  

Acetaminophen- (APAP-) induced hepatic injury is an important clinical challenge. Oxidative stress, inflammation, apoptosis, and endoplasmic reticulum stress (ERS) contribute to the pathogenesis. Methane has potential anti-inflammatory, antioxidant, and antiapoptotic properties. This project was aimed at studying the protective effects and relative mechanisms of methane in APAP-induced liver injury. In the in vivo experiment, C57BL/6 mice were treated with APAP (400 mg/kg) to induce hepatic injury followed by methane-rich saline (MRS) 10 ml/kg i.p. after 12 and 24 h. We observed that MRS alleviated the histopathological lesions in the liver, decreased serum aminotransferase levels, reduced the levels of inflammatory cytokines, suppressed the nuclear factor-κB expression. Further, we found that MRS relieved oxidative stress by regulating the Nrf2/HO-1/NQO1 signaling pathway and their downstream products after APAP challenge. MRS also regulated proteins associated with ERS-induced apoptosis. In the in vitro experiment, the L-02 cell line was treated with APAP (10 mM) to induce hepatic injury. We found that a methane-rich medium decreased the levels of reactive oxygen species (DHE fluorescent staining), inhibited apoptosis (cell flow test), and regulated the Nrf2/HO-1/NQO1 signaling pathway. Our data indicated that MRS prevented APAP-induced hepatic injury via anti-inflammatory, antioxidant, anti-ERS, and antiapoptotic properties involving the Nrf2/HO-1/NQO1 signaling pathway.


2010 ◽  
Vol 88 (5) ◽  
pp. 819-834 ◽  
Author(s):  
S. V. Rana ◽  
R. Pal ◽  
K. Vaiphei ◽  
R. P. Ola ◽  
K. Singh

This study evaluates the hepatoprotective effect of carotenoids against isoniazid (INH) and rifampicin (RIF). Thirty-six adult rats were divided into the following 4 groups: (1) control group treated with normal saline; (2) INH + RIF group treated with 50 mg·(kg body mass)–1·day–1 of INH and RIF each; (3) INH + RIF+ carotenoids group treated with 50 mg·(kg body mass)–1·day–1 of INH and RIF each and 10 mg·(kg body mass)–1·day–1 of carotenoids; and (4) carotenoids group treated with 10 mg·(kg body mass)–1·day–1 of carotenoids for 28 days intragastrically. Oxidative stress and antioxidant levels in liver and blood, liver histology and change in transaminases were measured in all the above-mentioned groups. There was an increase in lipid peroxidation with a reduction in thiols, catalase, and superoxide dismutase (SOD) in the liver and blood of rats accompanied by an increase in transaminases, bilirubin, and alkaline phosphatase. Treatment with carotenoids along with INH + RIF partially reversed lipid peroxidation, thiols, catalase, and SOD in the liver and blood of rats. Elevated levels of the enzymes in serum were also reversed partially by this treatment. The degree of necrosis, portal triaditis, and inflammation were also lowered in the carotenoids group. In conclusion, carotenoids supplementation in INH + RIF treated rats showed partial protection.


2011 ◽  
Vol 51 (3) ◽  
pp. 311-321 ◽  
Author(s):  
Borna Relja ◽  
Eva Töttel ◽  
Lara Breig ◽  
Dirk Henrich ◽  
Heinz Schneider ◽  
...  

2007 ◽  
Vol 361 (3) ◽  
pp. 670-674 ◽  
Author(s):  
Kei-ichi Fukuda ◽  
Sadamitsu Asoh ◽  
Masahiro Ishikawa ◽  
Yasuhiro Yamamoto ◽  
Ikuroh Ohsawa ◽  
...  

2021 ◽  
Author(s):  
Mahmoud El Sayed Habieb ◽  
Marwa Abd El Hameed Mohamed ◽  
Doaa Mohamed ElGamal ◽  
Asrar Mohamed Hawas ◽  
Tarek Mohamed Mohamed

Abstract This work aims to investigate the possible inhibitory action of β-hydroxybutyrate (βOHB) against hematological alterations and hepatic injury associated with oxidative stress caused by D-galactose or γ-irradiation in rats. Six groups of male rats were used as the control, irradiated group (5 Gy), D-galactose (150 mg/kg b.wt), β-hydroxybutyrate (72.8 mg/kg b.wt), γ-irradiation plus βOHB, and D-galactose plus βOHB. Complete blood count and glucose-6-phosphate-dehydrogenase (G6PD) activity were determined in whole-blood samples. In addition, the hepatic malondialdehyde (MDA), nitric oxide (NO), and glutathione (GSH) levels and the superoxide dismutase (SOD) activity were evaluated. Moreover, certain elements were measured in liver tissue (iron (Fe), copper (Cu), and zinc (Zn)). The G6PD activity significantly diminished post exposure to D-galactose or γ-irradiation. In the βOHB, D-galactose, or γ-irradiation groups, liver MDA levels and SOD activity were significantly increased. Meanwhile, NO and GSH levels were significantly increased relative to normal control levels in the γ-irradiation group. The findings showed that βOHB alleviated hematological alterations, enhanced the altered biochemical indices, and modulated the change in Cu, Fe, and Zn elements in D-galactose or γ-irradiation group. These results highlight the role of βOHB as a powerful protective agent against hematological alterations and liver impairment by reducing G6PD-mediated oxidative stress and controlling the measured elements.


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