Protective effect of Allicin on intestinal mucosal barrier of septic rats

Abstract

Objective To investigate the protective effect of allicin on intestinal mucosal barrier of septic rats so as to explore the possible mechanism. Methods Twenty-four male SD rats were randomly (random number)divided into sham, septic model and allicin treatment group. Septic model was established by cecal ligation and puncture (CLP) in rats. Rats in the treatment group were administered with allicin (30 mg/kg, ip) at 6 h and 12 h after modeling, while those in the model and sham groups were treated with equal amount of saline instead. Rats were sacrificed at 24 h and the serum D-lactic acid, diamine oxidase (DAO) and fluorescence isothiocyanate-dextran (FITC-Dextran, FD-40) were determined to evaluate the intestinal mucosal barrier function. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), and the activity of superoxide dismutase (SOD) in intestinal tissue were measured. Histopathological changes of intestinal mucosa injury were assessed by Hematoxylin-eosin staining. Results Compared with the sham group, levels of serum D-lactic acid, DAO and FD-40 increased significantly in the CLP group (D-lactic acid: 599.4±101.1 vs. 149.2±20.63 nmol/mL, t=11.84, P<0.01; DAO: 302.1±64.5 vs. 76.57±14.76 ng/mL, t=9.433, P<0.01; FD-40: 6664.0±1437.0 vs. 1446.0±205.0 ng/mL, t=9.704, P<0.01); intestinal morphology damage occurred in the CLP group; intestinal levels of TNF-α, IL-6 and MDA increased greatly (TNF-α: 186.35±20.43 vs. 58.76±8.94 pg/mL, t=17.23, P<0.01; IL-6: 763.25±85.23 vs. 125.36±14.37 pg/mL, t=22.54, P<0.01; MDA: 29.36±3.27 vs. 7.24±0.85 nmol/mg prot, t=16.61, P<0.01), while SOD activity reduced (35.75±6.53 vs. 73.26±8.35 U/mg prot, t=10.57, P<0.01) in the CLP group. Allicin treatment greatly inhibited the increase of D-lactic acid, DAO and FD-40 levels in rat plasma caused by CLP (D-lactic acid: 330.1±81.77 vs. 599.4±101.1 nmol/mL, t=7.086, P<0.01; DAO: 171.8±49.70 vs. 302.1±64.56 ng/mL, t=5.45, P<0.01; FD-40: 3349.0±1167.0 vs. 6664.0±1437.0 ng/mL, t=6.165, P<0.01); intestinal morphology damage was improved in the allicin treatment group; allicin treatment greatly inhibited the intestinal levels of TNF-α, IL-6 and MDA and preserved the intestinal SOD activity compared with the CLP group (TNF-α: 95.37±12.68 vs. 186.35±20.43 pg/mL, t=12.29, P<0.01; IL-6: 354.27±46.27 vs. 763.25±85.23 pg/mL, t=14.45, P<0.01; MDA: 16.27±3.14 vs. 29.36±3.27 nmol/mg prot, t=9.831, P<0.01; SOD: 55.35±6.23 vs. 35.75±6.53 U/mg prot, t=5.522, P<0.01). Conclusions Allicin could inhibit local inflammation and oxidative stress in the intestine and exerts protective effect on intestinal mucosal barrier of septic rats. Key words: Allicin; Sepsis; Intestinal mucosal barrier; D-lactic acid; Diamine oxidase; Fluorescein isothiocyanate-dextran; Inflammation; Oxidative stress