Liver ischemia-reperfusion injury (IRI) is a common clinical event with high morbidity in patients undergoing complex liver surgery or having abdominal trauma. Inflammatory and oxidative stress responses are the main contributing factors in liver IRI. The iridoid glucoside aucubin (AU) has good anti-inflammatory and antioxidative effects; however, there are no relevant reports on the protective effect of glucosides on hepatic IRI. The purpose of this study was to determine whether AU pretreatment could prevent liver IRI and to explore the mechanism. Sprague-Dawley rats were randomly divided into five groups. The sham operation and IRI control groups were given intraperitoneal injections of normal saline, while the AU low-dose (AU-L) group, AU medium-dose (AU-M) group, and AU high-dose (AU-H) group were given intraperitoneal injections of AU at doses of 1, 5, and 10 mg/kg/day, respectively. After 10 d, liver IRI (70% liver ischemia for 1 h, reperfusion for 6 h) was surgically established in all groups except the sham group. Our results confirmed that liver injury was significantly aggravated after hepatic ischemia-reperfusion. AU alleviated the increase of transaminase and pathological changes induced by ischemia-reperfusion and improved liver damage. AU could also ameliorate the inflammatory and oxidative stress responses induced by ischemia-reperfusion and reduced expression of high mobility group protein (HMG)B1, receptor for advanced glycation end-products (RAGE), tumor necrosis factor (TNF)-a, interleukin (IL)-1b, and reactive oxygen species (ROS). Moreover, AU reduced ischemia-reperfusion-induced mitochondrial dysfunction and cells apoptosis, increased peroxisome proliferatoractivated receptor g coactivator (PGC)-1a and uncoupling (UCP)2 protein expression, and reduced caspase-3, cleaved caspase-3, and Cytochrome P450 proteins (CYP) expression. To determine expression levels of the Toll-like receptor (TLR)-4/ nuclear factor-kB (NF-kB) pathway-related proteins in vitro and in vivo, we also measured TLR-4, myeloid differentiation factor88 (MyD88), NF-kB P65, p-P65, Ikappa-B-alpha (IkB-a), and p-IkB-a levels. The results showed that AU effectively

Eucommia ulmoides polysaccharide (EUP) has been shown to have anti-inflammatory and antioxidant effects. However, the mechanism underlying these effects has rarely been reported, and whether EUP can reduce liver injury in hepatic ischemia-reperfusion injury (HIRI) has not been reported. In this study, 40 Sprague-Dawley (SD) rats were randomly divided into 5 groups: the sham group, ischemia-reperfusion (I/R) group, and three EUP pretreatment groups (320 mg/kg, 160 mg/kg, and 80 mg/kg). SD rats were pretreated with EUP by gavage once a day prior to I/R injury for 10 days. Except for the sham group, blood flow in the middle and left liver lobes was blocked in all the other groups, resulting in 70% liver ischemia, and the ischemia and reperfusion times were 1 h and 4 h, respectively. Ischemic liver tissue and serum were obtained to detect biochemical markers and liver histopathological damage. Compared with the I/R group, after EUP pretreatment, serum alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor-α, and interleukin-1β levels were significantly decreased, malondialdehyde levels in liver tissues were significantly decreased, superoxide dismutase levels were significantly increased, and the area of liver necrosis was notably reduced. To understand the specific mechanism involved, we determined the levels of Toll-like receptor- (TLR-) 4-nuclear factor-kappaB (NF-κB) pathway-associated proteins in vivo and in vitro. The data showed that EUP can reduce liver damage by decreasing ROS levels and inhibiting TLR-4-NF-κB pathway activation and may be a promising drug in liver surgery to prevent HIRI.

Han et al.: Protective Effects of Smilax glabra Roxb on CCl4 Induced Rat ALI by Inhibiting NLRP3The experiment was conducted to investigate the protective effect of Smilax glabra Roxb. aqueous extract on carbon tetrachloride induced acute liver injury in rats by regulating the nucleotide binding leucine rich repeat receptors family pyrin domain containing 3 inflammasome. In this study, a rat acute liver injury model was established by a single intraperitoneal injection of 50 % carbon tetrachloride oil solution (1 ml/kg body weight). A total of 50 rats were randomly divided into control group, model group and 3 Smilax glabra Roxb. aqueous extract intervention groups (0.75, 1.5 and 3 g/kg body weight/d). Smilax glabra Roxb. aqueous extract or distilled water was orally administered by gavage once daily for seven consecutive days. Then the blood and liver samples were collected. The results showed that in the 3 intervention Smilax glabra Roxb. aqueous extract groups, the levels of serum aspartate aminotransferase and Alanine aminotransferase, the content of malondialdehyde in rat liver tissues significantly reduced and superoxide dismutase, catalase and glutathione increased significantly, the liver lobule structures were repaired and the liver cells were aligned in an orderly manner, the expressions of nucleotide binding leucine rich repeat receptors family pyrin domain containing 3 inflammasome, apoptosis associated speck like protein containing and caspase-1 proteins, Interleukin 1 beta messenger ribonucleic acid was decreased. Smilax glabra Roxb. aqueous extract exerted a protective effect against carbon tetrachloride induced acute liver injury by inhibiting the activation of nucleotide binding leucine rich repeat receptors family pyrin domain containing 3 inflammasome, which suggest a promising avenue for the exploration of Smilax glabra Roxb. aqueous extract in improving acute liver injury.