scholarly journals Arctigenin attenuates CCl4-induced hepatotoxicity through suppressing matrix metalloproteinase-2 and oxidative stress

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ghalia Mohamed Kanawati ◽  
Iqbal Hassan Al-Khateeb ◽  
Yasser Ibrahim Kandil

Abstract Background In spite of the huge advances in recent medicine, there is no effective drug that completely protects the liver from toxic materials. This study was conducted to investigate the hepatoprotective effect of arctigenin from burdock (Arctium lappa) against carbon tetrachloride (CCl4)-induced liver injury. Results Arctigenin pre-administration reduced hepatotoxicity markers significantly as compared to CCl4 group. In addition, both silymarin and arctigenin declined matrix metalloproteinase-2 (MMP-2) in the serum (1177 ± 176), (978 ± 135) significantly as compared to CCl4 group (1734 ± 294). The hepatic antioxidant parameters (total glutathione, superoxide dismutase, and glutathione reductase) were significantly decreased after CCl4 injection, an effect that has been prevented by pre-administration of both silymarin and arctigenin. Histological examinations illustrated that arctigenin reduced CCl4 damage, where it decreased inflammation, congestion, and ballooning. Conclusions Arctigenin exerted a hepatoprotective effect against CCl4-induced liver damage in terms of suppressing MMP-2 and oxidative stress comparative to that of silymarin.

Life Sciences ◽  
2016 ◽  
Vol 157 ◽  
pp. 125-130 ◽  
Author(s):  
Vinicius P. Garcia ◽  
Helena N.M. Rocha ◽  
Gustavo M. Silva ◽  
Tatiana A.G. Amaral ◽  
Niels H. Secher ◽  
...  

Author(s):  
Paulina Nguyen-Powanda ◽  
Bernard Robaire

Abstract The efficiency of antioxidant defense system decreases with aging, thus resulting in high levels of reactive oxygen species (ROS) and DNA damage in spermatozoa. This damage can lead to genetic disorders in the offspring. There are limited studies investigating the effects of the total loss of antioxidants, such as superoxide dismutase-1 (SOD1), in male germ cells as they progress through spermatogenesis. In this study, we evaluated the effects of aging and removing SOD1 (in male germ cells of SOD1-null (Sod1−/−) mice) in order to determine the potential mechanism(s) of DNA damage in these cells. Immunohistochemical analysis showed an increase in lipid peroxidation and DNA damage in the germ cells of aged wild-type (WT) and Sod1−/− mice of all age. Immunostaining of OGG1, a marker of base excision repair (BER), increased in aged WT and young Sod1−/− mice. In contrast, immunostaining intensity of LIGIV and RAD51, markers of non-homologous end-joining (NHEJ) and homologous recombination (HR), respectively, decreased in aged and Sod1−/− mice. Gene expression analysis showed similar results with altered mRNA expression of these key DNA repair transcripts in pachytene spermatocytes and round spermatids of aged and Sod1−/− mice. Our study indicates that DNA repair pathway markers of BER, NHEJ, and HR are differentially regulated as a function of aging and oxidative stress in spermatocytes and spermatids, and aging enhances the repair response to increased oxidative DNA damage, whereas impairments in other DNA repair mechanisms may contribute to the increase in DNA damage caused by aging and the loss of SOD1.


2004 ◽  
Vol 279 (29) ◽  
pp. 29938-29943 ◽  
Author(s):  
Laran T. Jensen ◽  
Raylene J. Sanchez ◽  
Chandra Srinivasan ◽  
Joan Selverstone Valentine ◽  
Valeria Cizewski Culotta

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