Potential Hepatoprotective Effects of Allicin on Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Oxidative Stress, Inflammation, and Apoptosis.

The global burden of liver disease is enormous, which highlights the need for effective hepatoprotective agents. It was reported that allicin exhibits protective effects against a range of diseases. In this study, we further evaluated allicin's effect and mechanism in acute hepatic injury. Liver injury in mice was induced by intraperitoneal injection with 1% CCl4 (10 mL/kg/day). When the first dose was given, CCl4 was given immediately after administration of different doses of allicin (40, 20, and 10 mg/kg/day) as well as compound glycyrrhizin (CGI, 80 mg/kg/day), and then different doses of allicin (40, 20, and 10 mg/kg/day) as well as compound glycyrrhizin (CGI, 80 mg/kg/day) were administrated every 12 h. The animals were dissected 24 h after the first administration. The findings demonstrated a significant inhibition of CCl4-induced acute liver injury following allicin treatment. This inhibition was evidenced by notable reductions in serum levels of transaminases, specifically aspartate transaminase, along with mitigated histological damage to the liver. In this protective process, allicin plays the role of reducing the amounts or the expression levels of proinflammatory cytokines, IL-1ß, IL-6. Furthermore, allicin recovered the activities of the antioxidant enzyme catalase (CAT) and reduced the production of malondialdehyde (MDA) in a dose-dependent manner, and also reduced liver Caspase 3, Caspase 8, and BAX to inhibit liver cell apoptosis. Further analysis showed that the administration of allicin inhibited the increased protein levels of Nuclear factor-erythroid 2-related factor 2 (Nrf2) and NAD(P)H:quinone oxidoreductase 1 (NQO1), which is related to inflammation and oxidative stress. The in vitro study of the LPS-induced RAW264.7 inflammatory cell model confirmed that allicin can inhibit important inflammation-related factors and alleviate inflammation. This research firstly clarified that allicin has a significant protective effect on CCl4-induced liver injury via inhibiting the inflammatory response and hepatocyte apoptosis, alleviating oxidative stress associated with the progress of liver damage, highlighting the potential of allicin as a hepatoprotective agent.

Allicin affects the pharmacokinetics of sulfadiazine and florfenicol by downregulating the expression of jejunum P-gp and BCRP in broilers.

Allicin, one of the main bioactive compounds in garlic, is an excellent feed additive. It is unknown whether allicin affects the expression of P-gp and BCRP, 2 important ABC efflux transporters related to the pharmacokinetics of antimicrobials in chickens. In this study, by bidirectional transport test and broiler jejunum in situ perfusion, we found that allicin inhibited the efflux transport of P-gp and BCRP for their substrates sulfadiazine and florfenicol, 2 commonly used antimicrobials in broilers. Furthermore, we observed that allicin decreased the mRNA expression of chicken jejunum P-gp and BCRP. Pretreatment with allicin changed the pharmacokinetic behavior of orally administered sulfadiazine, by increasing AUC (41.85 vs. 31.24, P < 0.01) and Cmax values (9.82 vs. 8.40, P < 0.05) and decreasing CLZ (0.45 vs. 0.62, P < 0.01). Similarly, pretreatment with allicin also altered pharmacokinetics of orally administered florfenicol, by increasing AUC (18.38 vs. 13.52, P < 0.01) and decreasing CLZ. The results indicate that allicin could inhibit jejunum P-gp and BCRP expression and efflux function, thereby increasing the plasma concentrations of their substrates in broilers.

Identification of a novel bacterial taxon associated with bovine mastitis showing a close evolutionary relationship with Elizabethkingia sp.

Recently, the characteristics of prevalent bacterial pathogens causing bovine mastitis have become increasingly complicated, and many commensal or unusual bacterial species have been isolated from milk samples of cows with mastitis. Strain JS20170427COW was isolated dominantly from the milk of Holstein Friesian cows with mastitis in Jiangsu province in China. Colonies of this strain showed a hillock-like protrusion, with a pale-yellow color at the protrusion and a transparent edge, 4-5 mm in diameter after cultivation at 37 °C for 24 h on 5% sheep blood-enriched agar. Although 16 s rRNA analysis showed the closest relationship with the family Flavobacteriaceae containing Elizabethkingia spp., Riemerella sp. and Soonwooa buanensis, the bacterial species of strain JS20170427COW could not be identified adequately because it had a sequence identity of less than 95 % in 16 s rRNA when compared with all the known species of the family Flavobacteriaceae. Unexpectedly, both the first and re-sequencing data determined the whole genome size of strain JS20170427COW to be 2.69 Mb, which is different from the above three closest bacterial species. Therefore, we hypothesized that strain JS20170427COW is a novel taxon of Flavobacteriaceae. Further identification using conserved genes, single-nucleotide polymorphisms (SNPs), phylogenetic and average nucleotide identity analyses based on whole genome data suggested that JS20170427COW was more likely to be an Elizabethkingia-like strain, but that it does not belong to the Elizabethkingia genus. Comparison of the predicted open reading frames (ORFs) revealed that strain JS20170427COW encodes more special genes than Elizabethkingia species. In summary, we identified a novel Flavobacteriaceae taxon showing a close relationship with Elizabethkingia subspecies, which has potential pathogenicity in bovine mastitis.