Tags

Type your tag names separated by a space and hit enter

Notoginsenoside R1 attenuates renal ischemia-reperfusion injury in rats.
Shock. 2010 Sep; 34(3):314-20.S

Abstract

Ischemia-reperfusion (I/R) injury of the kidney is a complex pathophysiological process and a major cause of acute renal failure. It has been shown that I/R injury is related to inflammatory responses and activation of apoptotic pathways. Inhibition of certain elements of inflammatory responses and apoptotic pathway seemed to ameliorate renal I/R injury. As an effective element of Panax notoginseng, NR1 has antioxidant, anti-inflammatory, antiapoptotic, and immune-stimulatory activities. Therefore, we speculate that NR1 can attenuate renal I/R injury. Ischemia-reperfusion injury was induced by renal pedicle ligation followed by reperfusion along with a contralateral nephrectomy. Male Sprague-Dawley rats were randomized to four groups: sham group, I/R control group, NR1-1 group (rats treated with NR1, 20 mg.kg.d) and NR1-2 group (rats treated with NR1, 40 mg.kg.d). All animals were killed 72 h after I/R induction. Blood and renal tissues were collected. Renal dysfunction was observed by the level of serum creatinine and histological evaluation. Apoptosis and inflammatory response in the tissue of kidney were detected mainly with molecular biological methods. NR1 attenuated I/R-induced renal dysfunction as indicated by the level of serum creatinine and histological evaluation. It prevented the I/R-induced increases in the levels of proinflammatory cytokine TNF-alpha, myeloperoxidase activity, phosphorylation of p38, and activation of nuclear factor kappaB with cell apoptosis in the kidney and enhanced expression of antiapoptosis cytokine bcl-2. Treatment with NR1 improves renal function after I/R associated with a significant reduction in cell apoptosis and inflammatory responses, which may be related to p38 and nuclear factor kappaB inhibition.

Authors+Show Affiliations

Department of Burn Surgery, Changhai Hospital, Second Military Medical University, Shanghai, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20023602

Citation

Liu, Wen-Jun, et al. "Notoginsenoside R1 Attenuates Renal Ischemia-reperfusion Injury in Rats." Shock (Augusta, Ga.), vol. 34, no. 3, 2010, pp. 314-20.
Liu WJ, Tang HT, Jia YT, et al. Notoginsenoside R1 attenuates renal ischemia-reperfusion injury in rats. Shock. 2010;34(3):314-20.
Liu, W. J., Tang, H. T., Jia, Y. T., Ma, B., Fu, J. F., Wang, Y., Lv, K. Y., & Xia, Z. F. (2010). Notoginsenoside R1 attenuates renal ischemia-reperfusion injury in rats. Shock (Augusta, Ga.), 34(3), 314-20. https://doi.org/10.1097/SHK.0b013e3181ceede4
Liu WJ, et al. Notoginsenoside R1 Attenuates Renal Ischemia-reperfusion Injury in Rats. Shock. 2010;34(3):314-20. PubMed PMID: 20023602.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Notoginsenoside R1 attenuates renal ischemia-reperfusion injury in rats. AU - Liu,Wen-Jun, AU - Tang,Hong-Tai, AU - Jia,Yi-Tao, AU - Ma,Bing, AU - Fu,Jin-Feng, AU - Wang,Yu, AU - Lv,Kai-Yang, AU - Xia,Zhao-Fan, PY - 2009/12/22/entrez PY - 2009/12/22/pubmed PY - 2011/2/16/medline SP - 314 EP - 20 JF - Shock (Augusta, Ga.) JO - Shock VL - 34 IS - 3 N2 - Ischemia-reperfusion (I/R) injury of the kidney is a complex pathophysiological process and a major cause of acute renal failure. It has been shown that I/R injury is related to inflammatory responses and activation of apoptotic pathways. Inhibition of certain elements of inflammatory responses and apoptotic pathway seemed to ameliorate renal I/R injury. As an effective element of Panax notoginseng, NR1 has antioxidant, anti-inflammatory, antiapoptotic, and immune-stimulatory activities. Therefore, we speculate that NR1 can attenuate renal I/R injury. Ischemia-reperfusion injury was induced by renal pedicle ligation followed by reperfusion along with a contralateral nephrectomy. Male Sprague-Dawley rats were randomized to four groups: sham group, I/R control group, NR1-1 group (rats treated with NR1, 20 mg.kg.d) and NR1-2 group (rats treated with NR1, 40 mg.kg.d). All animals were killed 72 h after I/R induction. Blood and renal tissues were collected. Renal dysfunction was observed by the level of serum creatinine and histological evaluation. Apoptosis and inflammatory response in the tissue of kidney were detected mainly with molecular biological methods. NR1 attenuated I/R-induced renal dysfunction as indicated by the level of serum creatinine and histological evaluation. It prevented the I/R-induced increases in the levels of proinflammatory cytokine TNF-alpha, myeloperoxidase activity, phosphorylation of p38, and activation of nuclear factor kappaB with cell apoptosis in the kidney and enhanced expression of antiapoptosis cytokine bcl-2. Treatment with NR1 improves renal function after I/R associated with a significant reduction in cell apoptosis and inflammatory responses, which may be related to p38 and nuclear factor kappaB inhibition. SN - 1540-0514 UR - https://www.unboundmedicine.com/medline/citation/20023602/Notoginsenoside_R1_attenuates_renal_ischemia_reperfusion_injury_in_rats_ L2 - https://doi.org/10.1097/SHK.0b013e3181ceede4 DB - PRIME DP - Unbound Medicine ER -