Hepatoprotective effect of sodium hydrosulfide on hepatic encephalopathy in rats

被引:13
作者
Kwon, Kyoung Wan [1 ]
Nam, Yoonjin [1 ]
Choi, Won Seok [1 ]
Kim, Tae Wook [1 ]
Kim, Geon Min [1 ]
Sohn, Uy Dong [1 ]
机构
[1] Chung Ang Univ, Coll Pharm, Dept Pharmacol, Seoul 06974, South Korea
基金
新加坡国家研究基金会;
关键词
Hepatic encephalopathy; Hydrogen sulfide; Inflammation; HYDROGEN-SULFIDE; NMDA RECEPTOR; LIVER-CIRRHOSIS; NITRIC-OXIDE; AMMONIA; SUBUNIT; MODEL; HYPERAMMONEMIA; PATHOGENESIS; MODULATION;
D O I
10.4196/kjpp.2019.23.4.263
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Hydrogen sulfide is well-known to exhibit anti-inflammatory and cyto-protective activities, and also has protective effects in the liver. This study aimed to examine the protective effect of hydrogen sulfide in rats with hepatic encephalopathy, which was induced by mild bile duct ligation. In this rat model, bile ducts were mildly ligated for 26 days. Rats were treated for the final 5 days with sodium hydrosulfide (NaHS). NaHS (25 mu mol/kg), 0.5% sodium carboxymethyl cellulose, or silymarin (100 mg/kg) was administered intraperitoneally once per day for 5 consecutive days. Mild bile duct ligation caused hepatotoxicity and inflammation in rats. Intraperitoneal NaHS administration reduced levels of aspartate aminotransferase and alanine aminotransferase, which are indicators of liver disease, compared to levels in the control mild bile duct ligation group. Levels of ammonia, a major causative factor of hepatic encephalopathy, were also significantly decreased. Malondialdehyde, myeloperoxidase, catalase, and tumor necrosis factor-alpha levels were measured to confirm antioxidative and anti-inflammatory effects. N-Methyl-D-aspartic acid (NMDA) receptors with neurotoxic activity were assessed for subunit NMDA receptor subtype 2B. Based on these data, NaHS is suggested to exhibit hepatoprotective effects and guard against neurotoxicity through antioxidant and anti-inflammatory actions.
引用
收藏
页码:263 / +
页数:9
相关论文
共 42 条
[11]   Hepatic encephalopathy in liver cirrhosis - Pathogenesis, diagnosis and management [J].
Gerber, T ;
Schomerus, H .
DRUGS, 2000, 60 (06) :1353-1370
[12]   Rats with Mild Bile Duct Ligation Show Hepatic Encephalopathy with Cognitive and Motor Impairment in the Absence of Cirrhosis: Effects of Alcohol Ingestion [J].
Gimenez-Garzo, Carla ;
Salhi, Dounia ;
Urios, Amparo ;
Ruiz-Sauri, Amparo ;
Carda, Carmen ;
Montoliu, Carmina ;
Felipo, Vicente .
NEUROCHEMICAL RESEARCH, 2015, 40 (02) :230-240
[13]   Hepatic Encephalopathy [J].
Gow, Adam G. .
VETERINARY CLINICS OF NORTH AMERICA-SMALL ANIMAL PRACTICE, 2017, 47 (03) :585-+
[14]   SUPPRESSION OF CELLULAR-IMMUNITY IN OBSTRUCTIVE-JAUNDICE IS CAUSED BY ENDOTOXINS - A STUDY WITH GERM-FREE RATS [J].
GREVE, JW ;
GOUMA, DJ ;
SOETERS, PB ;
BUURMAN, WA .
GASTROENTEROLOGY, 1990, 98 (02) :478-485
[15]   Modulation of sulfide oxidation and toxicity in rat mitochondria by dehydroascorbic acid [J].
Hildebrandt, Tatjana M. .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2011, 1807 (09) :1206-1213
[16]   Ammonia and amino acid profiles in liver cirrhosis: Effects of variables leading to hepatic encephalopathy [J].
Holecek, Milan .
NUTRITION, 2015, 31 (01) :14-20
[17]   Oxidative-stress-related changes in the livers of bile-duct-ligated rats [J].
Huang, YT ;
Hsu, YC ;
Chen, CJ ;
Liu, CT ;
Wei, YH .
JOURNAL OF BIOMEDICAL SCIENCE, 2003, 10 (02) :170-178
[18]   The protective mechanism of QGC in feline esophageal epithelial cells by interleukin-1β treatment [J].
Jang, Hyun Soo ;
Um, Seung In ;
Lee, Sung Hee ;
Whang, Wan Kyunn ;
Min, Young Sil ;
Park, Sun Young ;
Sohn, Uy Dong .
ARCHIVES OF PHARMACAL RESEARCH, 2017, 40 (02) :204-213
[19]   Ammonia metabolism and hepatic encephalopathy [J].
Katayama, K .
HEPATOLOGY RESEARCH, 2004, 30 :S71-S78
[20]   Phosphatidylcholine attenuated docetaxel-induced peripheral neurotoxicity in rats [J].
Kim, Sung Tae ;
Kyung, Eun Jung ;
Suh, Jung Sook ;
Lee, Ho Sung ;
Lee, Jun Ho ;
Chae, Soo In ;
Park, Eon Sub ;
Chung, Yoon Hee ;
Bae, Jinhyung ;
Lee, Tae Jin ;
Lee, Won Mo ;
Sohn, Uy Dong ;
Jeong, Ji Hoon .
DRUG AND CHEMICAL TOXICOLOGY, 2018, 41 (04) :476-485