Therapeutic effects of Lactobacillus casei Qian treatment in activated carbon-induced constipated mice

Mol Med Rep. 2015 Aug;12(2):3191-9. doi: 10.3892/mmr.2015.3737. Epub 2015 May 6.

Abstract

In the present study, the therapeutic effects of Lactobacillus casei Qian (LC-Qian), the key microorganism in Tibetan yak yoghurt, on activated carbon-induced constipation were determined in vivo. ICR mice were treated with LC-Qian for nine days by oral administration. The body weight, defecation status, gastrointestinal transit and defecation time of mice were assessed, and the serum levels of motilin (MTL), gastrin (Gas), endothelin (ET), somatostatin (SS), acetylcholinesterase (AChE), substance P (SP) and vasoactive intestinal peptide (VIP) were further evaluated. Bisacodyl was used as the positive control. The time until the first black stool defecation following carbon intake of the normal, control, 100 mg/kg bisacodyl-treated, Lactobacillus bulgaricus (LB)-treated, LC-Qian (L)-and LC-Qian (H)-treated mice was 93, 231, 121, 194, 172 and 157 min, respectively. Following treatment with LC-Qian, the gastrointestinal transit was increased to 52.4% [LC-Qian (L)] and 65.8% [LC-Qian (H)], while that in the group treated with the common lactic acid bacteria of LB was 40.3%. The MTL, Gas, ET, AChE, SP and VIP serum levels were significantly increased and levels of SS were reduced in mice following LC-Qian treatment compared with those in the control mice (P<0.05). Reverse transcription quantitative polymerase chain reaction indicated that LC-Qian raised the c-Kit, GDNF as well as SCF mRNA expression levels and reduced the TRPV1 and NOS expression levels in tissue of the small intestine in mice. These results suggested that lactic acid bacteria prevent constipation in mice, among which LC-Qian was the most effective.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholinesterase / genetics
  • Acetylcholinesterase / metabolism
  • Animals
  • Body Weight / drug effects
  • Carbon
  • Constipation / chemically induced
  • Constipation / diet therapy*
  • Constipation / genetics
  • Constipation / physiopathology
  • Defecation / drug effects
  • Endothelins / genetics
  • Endothelins / metabolism
  • Female
  • GPI-Linked Proteins / genetics
  • GPI-Linked Proteins / metabolism
  • Gastrins / genetics
  • Gastrins / metabolism
  • Gastrointestinal Transit / drug effects
  • Gene Expression / drug effects*
  • Glial Cell Line-Derived Neurotrophic Factor / genetics
  • Glial Cell Line-Derived Neurotrophic Factor / metabolism
  • Intestine, Small / drug effects*
  • Intestine, Small / metabolism
  • Intestine, Small / physiopathology
  • Lacticaseibacillus casei / physiology*
  • Mice
  • Mice, Inbred ICR
  • Motilin / genetics
  • Motilin / metabolism
  • Probiotics / pharmacology*
  • Proto-Oncogene Proteins c-kit / genetics
  • Proto-Oncogene Proteins c-kit / metabolism
  • Somatostatin / genetics
  • Somatostatin / metabolism
  • Substance P / genetics
  • Substance P / metabolism
  • TRPV Cation Channels / genetics
  • TRPV Cation Channels / metabolism
  • Vasoactive Intestinal Peptide / genetics
  • Vasoactive Intestinal Peptide / metabolism

Substances

  • Endothelins
  • GPI-Linked Proteins
  • Gastrins
  • Glial Cell Line-Derived Neurotrophic Factor
  • TRPV Cation Channels
  • TRPV1 protein, mouse
  • Substance P
  • Vasoactive Intestinal Peptide
  • Somatostatin
  • Motilin
  • Carbon
  • Proto-Oncogene Proteins c-kit
  • Acetylcholinesterase
  • Ache protein, mouse