Anti-Malondialdehyde polyclonal antibody

Ethnopharmacological relevance: Baihe Wuyao decoction (BWD), a prescription of Traditional Chinese Medicines, composed of alum brownii var. viridulum Baker.(Lilii Bulbus) and Lindera aggregata (Sims) Kosterm. (Linderae Radix), has been used to treat epigastric pain and superficial gastritis for hundreds of years in China. Recently, some compounds obtained from Lilii Bulbus and Linderae Radix had active effects of hepatic protection or liver fibrosis alleviation. Thus, we aim to evaluate the effects of BWD on treatment of chronic liver injury and liver fibrosis induced by carbon tetrachloride (CCl4) and to elucidate the possible molecular mechanism. Materials and methods: Mice were treated with BWD (low, medium and high dose), diammonium glycyrrhizinate or vehicle by oral gavage once daily, simultaneously intraperitoneal injected with a single dose of CCl4 (1 mu l/g body weight) twice a week for consecutive 6 weeks. Next, all mice were sacrificed after fasted 12 h, and serums and liver tissues were harvested for analysis. The hepatic injury was detected by serum biomarker assay, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The hepatic histology and collagen were illustrated by hematoxylin-eosin staining and Sirius red staining respectively. The antioxidant capacity of liver tissues was evaluated by the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in liver homogenization. The mRNA gene or protein expressions related to fibrosis, oxidative stress and inflammation molecules were performed by real-time quantitative PCR (RT-PCR) or Western-blot. Results: BWD exhibited a good hepatic protection with ameliorating liver histological changes, decreasing serum AST and ALT contents, and reducing hepatic fibrosis with stimulation ECMs (such as Collagen1 and Collagen3) degradation. BWD inhibited hepatic stellate cells (HSCs) activation, promoted matrix metalloproteinase-2 (MMP2), MMP9, and MMP12 while suppressing tissue inhibitors of matrix metalloproteinase-1 (TIMP1) expression, and blocked traditional fibrosis TGF-beta 1/Smad2/3 signal pathway. Moreover, BWD exhibited antiinflammation effect proved by the reduction of liver Interleukin-1 beta (IL-1 beta), TNF-alpha, IL-11 mRNA levels and promoted anti-oxidation effects determined by inhibition of liver MDA and iNOS levels while promoting liver SOD and Mn-SOD. Conclusion: BWD ameliorates CCl4-induced CLI and liver fibrosis which is correlated to its blocking TGF-beta 1/Smad2/3 signaling, anti-inflammation, and anti-oxidation effects. BWD, as a small traditional prescription, is a promising treatment for CLI and liver fibrosis through multiple pharmacological targets.

The aim of the study was to investigate the protective effects of selenium yeast (SeY) against necroptosis triggered by Cd via inhibition of oxidative stress and MAPK pathway in the liver of chicken. Two hundred 120-day-old layers were randomly divided into four groups and raised for 120 days. The histopathological examination showed that necrosis characteristics were observed in Cd-exposed chicken livers. The exposure of Cd significantly reduced the activities of SOD, GSH-Px and CAT while improving MDA level in both serum and liver of chickens (P < 0.05), and induced oxidative stress. The MLKL, Rip1, RIP3, ERK, JNK and P38 mRNA expression of Cd group were significantly higher than other three groups (P < 0.01), and those in the Se + Cd group were significantly higher than control group and Se group (P < 0.01). However, the mRNA expression level of caspase8 of Cd was significantly lower than other three groups (P < 0.01), and that in the Se + Cd group was significantly higher than control group and Se group (P < 0.01), so the supplement of SeY could improve these situations. Similar results were also detected at the protein level. The results of the present study indicated that Cd could induce oxidative stress, activate MAPK pathway and evoke necroptosis damage in chicken livers, whereas SeY had protective effects in preventing this kind of Cd-induced injury by inhibition of oxidative stress and down-regulation MAPK pathway.