ABSTRACT
AIM: To investigate the role of reactive oxygen species ( ROS)-mediated mitochondrial oxidative injury in isonicotinyl hydrazide ( INH)-induced DNA damage and the protective effect of quercetin on L-02 cells.ME-THODS:The injury model of hepatocyte L-02cells in vitro induced by INH was established .The cells were divided into control group, INH group, low-dose quercetin group and high-dose quercetin group.The DNA damage of L-02 cells was evaluated by the comet test .The mitochondrion was prepared , and the level of mitochondrial ROS and the value of mitochondrial membrane potential (ΔΨm ) were detected by fluorescent probes DCFH-DA and rhodamine 123.The content of MDA was measured by TBA method .The activity of SOD was assessed with the xanthine oxidase method .The protein expression of Bcl-2 and Bax was determined by Western blotting , and the value of Bax/Bcl-2 was calculated .RESULTS:INH induced obvious DNA damage , increased the level of mitochondrial ROS , the content of MDA and the value of Bax/Bcl-2, and markedly reduced the value of ΔΨm and the activity of SOD in the L-02 cells.Quercetin attenuated DNA dam-age, reduced the level of mitochondrial ROS , elevated the value of ΔΨm , declined the content of MDA , increased the ac-tivity of SOD and decreased the value of Bax/Bcl-2 in the L-02 cells.CONCLUSION:INH induces DNA damage in L-02 cells by generation of mitochondrial oxidative stress .Quercetin has a protective effect on L-02 cells to attenuate the INH-in-duced DNA damage by inhibiting ROS-mediated mitochondrial oxidative damage .
ABSTRACT
Hedgehog pathway is an osteogenesis-related signaling pathway . During embryonic development , it regulates the growth and proliferation of progenitor cells and tissue formation. This pathway can be activated during liver injury. Activated Hedge-hog signaling pathway is involved in many aspects of liver wound-healing responses, including hepatic progenitor cell pro-liferation, myofibroblast transdifferentiation, apoptosis of various types of liver cells, inflammatory reactions, and vascular remod-eling. This article reviews the research progress in the role of Hedgehog signaling pathway in liver injury and the underlying mechanisms. The potential drug targets are also discussed. This review is to provide novel insights into antifibrotic research and therapeutic targets.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the mischief mechanism of oxidative stress in the varicocele (VC).</p><p><b>METHODS</b>Serum was taken from the spermatic and peripheral veins on ligation of the internal spermatic veins in 28 infertile males with VC. Experimental VC was established in male rats by partial ligation of the left renal vein. And testis tissue was taken three months after operation. The nitric oxide(NO), nitric oxide synthetase (NOS), xanthine oxidase (XO), lactic acid(Lac) and lactic dehydrogenase (LDH) in the serum of 28 infertile males with VC and the testis tissue of the VC rats were detected by spectrophotometry.</p><p><b>RESULTS</b>NO, NOS, XO and Lac in the serum of internal spermatic veins in the infertile males with VC were significantly higher than in the serum of peripheral veins in the VC patients (P < 0.01, P < 0.05). LDH was lower than that in peripheral serum. NO and XO of the left testis tissue in the VC rats were higher compared with the control group (P < 0.01). Lac in the left testis of the VC rats was lower than that in the control group rats (P < 0.01).</p><p><b>CONCLUSION</b>NO, NOS and XO in the serum of the VC patients and in the testis tissues of the VC rats were increased, and Lac and LDH were changed obviously, which might not only disturb spermatogenesis, but also inhibit sperm motility. Therefore they might be one of the causes of infertility in VC patients.</p>