Orally-pretreated LF41 attenuates LPS-induced TNF-α expression and hepatic injury.

<p><b>(A)</b> C57BL/6 mice (n = 8) either untreated or treated with antibiotic formula (Ab) were given single IP injection with LPS (500 μg/kg body weight). Mice were killed 2 and 16 h after LPS treatment for determination of hepatic TNF-α gene levels (left panel) by q-PCR and serum ALT activity (right panel), respectively. Results in the left panel are expressed as fold change relative to LPS. P > 0.05 compared to LPS. <b>(B)(C)</b> Mice (LPS-treated groups: n = 8–10 per group; the remainder: n = 6 per group) were given daily IG inoculation either for 10 consecutive days ofL-LF41, H-LF41, killed-LF41, LGG, BC41, or PBS, or for 21 consecutive days of either PBS or H-LF41 (right panel), and then single IP injection with LPS or PBS. Hepatic <i>Tnf</i> mRNA levels by q-PCR (B) and serum ALT activity (C) were determined. Results of (B) are expressed as fold change relative to PBS+PBS. H-LF41+LPS denotes 10 days of oral challenge with H-LF41 and then LPS injection, and other similar abbreviations conform to the same rule. * P < 0.05 compared to PBS+LPS. <b>(D)</b> Mice (LPS-treated groups: n = 8 per group; the remainder: n = 6 per group) were treated for 10 days with either PBS or H-LF41 and then challenged with LPS. Mice were killed 2 h after LPS treatment to test hepatic and serum TNF-α protein levels by ELISA.* P < 0.05 compared to PBS+LPS. <b>(E) (F)</b> Mice(LPS-treated groups: n = 12–14 per group; the remainder: n = 6–7 per group) pretreated for 10 days with PBS or H-LF were challenged with PBS or LPS. 20 h after the challenge, the inflammatory foci in the liver were determined (E), and representative histological outcomes of liver tissue were shown (F). * P < 0.05 compared to PBS+LPS. a: PBS+PBS; b: H-LF41+PBS; c: PBS+LPS; d: LF41+LPS. Values are shown as mean ± SEM. Results of <b>(A)</b> are representative of 2 experiments with similar results, and the remainder 3 experiments with similar results.