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The vitamin E derivative, EPC-K1, suppresses inflammation during hepatic ischemia-reperfusion injury and exerts hepatoprotective effects in rats.
J Surg Res. 2012 Jul; 176(1):164-70.JS

Abstract

BACKGROUND

An important component of postoperative management includes alleviation of hepatic ischemia-reperfusion (I/R) injury, which commonly results from liver surgery. EPC-K1 is a hydroxyl radical scavenger reported to have mitigating effects on I/R injury in many organs. This study evaluates the effects of EPC-K1 on hepatic I/R injury.

MATERIALS AND METHODS

Rats were injected subcutaneously with either EPC-K1 (100 mg/kg) or saline. The hepatic artery and left branch of the portal vein were clamped for 45 min under general anesthesia. Indicators of liver function, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH), and of liver tissue damage were evaluated after 6h and 24h of reperfusion. Serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and high-mobility group box 1 (HMGB1) protein were measured, and apoptosis was quantified via caspase 3/7 activity and TUNEL assay.

RESULTS

AST, ALT, and LDH levels increased significantly as a result of hepatic I/R injury, but were attenuated by EPC-K1 administration. Histologic findings revealed that normal structure of the hepatic parenchyma was maintained in rats pretreated with EPC-K1. TNF-α, IL-6, and HMGB1 levels rose significantly after reperfusion, together with activation of the inflammatory response. However, EPC-K1 administration suppressed levels of inflammatory markers and attenuated the inflammatory response. Moreover, EPC-K1 administration prevented apoptosis as determined by inhibition of caspase 3/7 activity and a decrease in apoptotic cells.

CONCLUSIONS

Results demonstrate that EPC-K1 inhibits the inflammatory response and suppresses apoptosis during hepatic I/R injury. This suggests that EPC-K1 has hepatoprotective effects, and may be a valuable and novel therapeutic agent in the clinical setting.

Authors+Show Affiliations

Beppu Medical Center, Beppu City, Oita, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22560539

Citation

Oishi, Kazushige, et al. "The Vitamin E Derivative, EPC-K1, Suppresses Inflammation During Hepatic Ischemia-reperfusion Injury and Exerts Hepatoprotective Effects in Rats." The Journal of Surgical Research, vol. 176, no. 1, 2012, pp. 164-70.
Oishi K, Hagiwara S, Koga S, et al. The vitamin E derivative, EPC-K1, suppresses inflammation during hepatic ischemia-reperfusion injury and exerts hepatoprotective effects in rats. J Surg Res. 2012;176(1):164-70.
Oishi, K., Hagiwara, S., Koga, S., Kawabe, S., Uno, T., Iwasaka, H., & Noguchi, T. (2012). The vitamin E derivative, EPC-K1, suppresses inflammation during hepatic ischemia-reperfusion injury and exerts hepatoprotective effects in rats. The Journal of Surgical Research, 176(1), 164-70. https://doi.org/10.1016/j.jss.2011.03.080
Oishi K, et al. The Vitamin E Derivative, EPC-K1, Suppresses Inflammation During Hepatic Ischemia-reperfusion Injury and Exerts Hepatoprotective Effects in Rats. J Surg Res. 2012;176(1):164-70. PubMed PMID: 22560539.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The vitamin E derivative, EPC-K1, suppresses inflammation during hepatic ischemia-reperfusion injury and exerts hepatoprotective effects in rats. AU - Oishi,Kazushige, AU - Hagiwara,Satoshi, AU - Koga,Satoko, AU - Kawabe,Satoshi, AU - Uno,Takahiro, AU - Iwasaka,Hideo, AU - Noguchi,Takayuki, Y1 - 2011/04/28/ PY - 2010/12/08/received PY - 2011/03/28/revised PY - 2011/03/31/accepted PY - 2012/5/8/entrez PY - 2012/5/9/pubmed PY - 2012/9/12/medline SP - 164 EP - 70 JF - The Journal of surgical research JO - J Surg Res VL - 176 IS - 1 N2 - BACKGROUND: An important component of postoperative management includes alleviation of hepatic ischemia-reperfusion (I/R) injury, which commonly results from liver surgery. EPC-K1 is a hydroxyl radical scavenger reported to have mitigating effects on I/R injury in many organs. This study evaluates the effects of EPC-K1 on hepatic I/R injury. MATERIALS AND METHODS: Rats were injected subcutaneously with either EPC-K1 (100 mg/kg) or saline. The hepatic artery and left branch of the portal vein were clamped for 45 min under general anesthesia. Indicators of liver function, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH), and of liver tissue damage were evaluated after 6h and 24h of reperfusion. Serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and high-mobility group box 1 (HMGB1) protein were measured, and apoptosis was quantified via caspase 3/7 activity and TUNEL assay. RESULTS: AST, ALT, and LDH levels increased significantly as a result of hepatic I/R injury, but were attenuated by EPC-K1 administration. Histologic findings revealed that normal structure of the hepatic parenchyma was maintained in rats pretreated with EPC-K1. TNF-α, IL-6, and HMGB1 levels rose significantly after reperfusion, together with activation of the inflammatory response. However, EPC-K1 administration suppressed levels of inflammatory markers and attenuated the inflammatory response. Moreover, EPC-K1 administration prevented apoptosis as determined by inhibition of caspase 3/7 activity and a decrease in apoptotic cells. CONCLUSIONS: Results demonstrate that EPC-K1 inhibits the inflammatory response and suppresses apoptosis during hepatic I/R injury. This suggests that EPC-K1 has hepatoprotective effects, and may be a valuable and novel therapeutic agent in the clinical setting. SN - 1095-8673 UR - https://www.unboundmedicine.com/medline/citation/22560539/The_vitamin_E_derivative_EPC_K1_suppresses_inflammation_during_hepatic_ischemia_reperfusion_injury_and_exerts_hepatoprotective_effects_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-4804(11)00315-5 DB - PRIME DP - Unbound Medicine ER -