<i>Lactobacillus acidophilus</i> attenuated TBI-mediated increase of MLCP.

<p>The interaction of <i>Lactobacillus acidophilus</i> and time on MLCP protein concentrations was not significant. (A) ELISA analysis showed that the concentrations of MLCP in intestinal smooth muscle were significantly increased after TBI, **<i>P</i> < 0.01 compared with control. <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated increase of MLCP, #<i>P</i> < 0.05 compared with TBI. (B) Immunohistochemistry analysis showed that marked increases in MLCP were observed in intestinal smooth muscle after TBI, and treatment with <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated increases of MLCP.</p

<i>P</i>-values of a two-way ANOVA for the effects of <i>Lactobacillus acidophilus</i>, time, and their interactions on the ten variables (N = 90).

<p>Note: MLCK: myosin light chain kinase; MLCP: myosin light chain phosphatase; PKC: protein kinase C; ICC numbers: the numbers of interstitial cells of Cajal.</p><p>*indicates a significant difference (<i>P</i> < 0.05)</p><p>**indicates a highly significant difference (<i>P</i> < 0.01).</p><p><i>P</i>-values of a two-way ANOVA for the effects of <i>Lactobacillus acidophilus</i>, time, and their interactions on the ten variables (N = 90).</p

<i>Lactobacillus acidophilus</i> restored the impaired ICC networks mediated by TBI.

<p>The ICC networks and numbers were detected under fluorescence microscope (400×) by immunofluorescence in ileal tissue sections. The interaction of <i>Lactobacillus acidophilus</i> and time on ICC numbers was not significant. (A) Low-density of ICC networks was observed after TBI compared with control. <i>Lactobacillus acidophilus</i> significantly restored TBI-mediated disruption of ICC networks. (B) The reduction of ICC numbers was also observed after TBI, **<i>P</i> < 0.01 compared with control. <i>Lactobacillus acidophilus</i> significantly restored TBI-mediated reduction of ICC numbers, #<i>P</i> < 0.05 compared with TBI.</p

<i>Lactobacillus acidophilus</i> could increase the MLC₂₀ phosphorylation.

<p>The interaction of <i>Lactobacillus acidophilus</i> and time on MLC₂₀ phosphorylation was not significant. (A and B) The levels of phospho-MLC₂₀ in intestinal smooth muscle were significantly decreased after TBI, *<i>P</i> < 0.05 compared with control. Treating with <i>Lactobacillus acidophilus</i> attenuated TBI-mediated inhibition of MLC₂₀ phosphorylation, #<i>P</i> < 0.05 compared with TBI. (C) The marked decreases in immunoreactivity for phospho-MLC₂₀ were observed in intestinal smooth muscle after TBI, and treatment with <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated inhibition of MLC₂₀ phosphorylation.</p

<i>Lactobacillus acidophilus</i> improved the contractile activity of intestinal smooth muscle impaired by TBI.

<p>Ninety C57BL/6 mice were randomly divided into three groups including control, TBI and TBI + <i>Lactobacillus acidophilus</i> groups. The interaction of <i>Lactobacillus acidophilus</i> and time on intestinal contractile activity was not significant. (A) The contractile activity was determined by histologic and physiologic analyses. (B) The average contractile amplitude was decreased after TBI, **<i>P</i> < 0.01 compared with control. <i>Lactobacillus acidophilus</i> could increase in contractile amplitude, #<i>P</i> < 0.05 compared with TBI. (C and D) The contractile frequency and tension were also decreased after TBI, **<i>P</i> < 0.01 compared with control. <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated decreases of contractile frequency and tension, #<i>P</i> < 0.05 compared with TBI. (E) The intestinal transit rate was decreased after TBI, **<i>P</i> < 0.01 compared with control. <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated decrease of intestinal transit rate, ##<i>P</i> < 0.01 compared with TBI.</p

<i>Lactobacillus acidophilus</i> attenuated TBI-mediated reduction of MLCK.

<p>The interaction of <i>Lactobacillus acidophilus</i> and time on MLCK protein concentrations was not significant. (A) ELISA analysis showed that the concentrations of MLCK in intestinal smooth muscle were significantly decreased after TBI, *<i>P</i> < 0.05 compared with control. <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated reduction of MLCK concentrations, ##<i>P</i> < 0.01 compared with TBI. (B) Immunohistochemistry analysis showed that marked decreases in MLCK were observed in intestinal smooth muscle after TBI, and treatment with <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated inhibition of MLCK.</p

<i>Lactobacillus acidophilus</i> improved the morphology of villus.

<p>The intestinal sections from control mice presented intact structures with complete intestinal mucosae and villi (3A, 3D and 3G). TBI caused abnormal intestinal wall morphology and damaged the intestinal villi and structural integrity (3B, 3E and 3H). <i>Lactobacillus acidophilus</i> recovered intestinal mucosae and restructured villi (3C, 3F and 3I).</p

<i>Lactobacillus acidophilus</i> attenuated TBI-mediated decrease in levels of phospho-MYPT1 and increases in PKC protein concentrations.

<p>The interaction of <i>Lactobacillus acidophilus</i> and time on phospho-MYPT1 concentrations was not significant. (A and B) A marked decreases in phospho-MYPT1 were observed in intestinal smooth muscle after TBI, **<i>P</i> < 0.01 compared with control. Treatment with <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated inhibition of MYPT1 phosphorylation, ##<i>P</i> < 0.01 compared with TBI. The interaction of <i>Lactobacillus acidophilus</i> and time on PKC protein concentrations was significant. (C) ELISA analysis showed that the concentrations of PKC were increased in intestinal smooth muscle after TBI, *<i>P</i> < 0.05 compared with control. <i>Lactobacillus acidophilus</i> significantly attenuated TBI-mediated induction of PKC protein concentrations, #<i>P</i> < 0.05 compared with TBI.</p