Abdominal Massage Reduces Visceral Hypersensitivity via Regulating GDNF and PI3K/AKT Signal Pathway in a Rat Model of Irritable Bowel Syndrome.
Bo LiXiong-Fei LuoSi-Wen LiuNa ZhaoHua-Nan LiWei ZhangYing-Ying ChenAn BaoJin-Gui WangQiang-Song WangPublished in: Evidence-based complementary and alternative medicine : eCAM (2020)
Changes in gut motility and visceral hypersensitivity are two major features of irritable bowel syndrome (IBS). Current drug treatments are often poorly efficacious, with many side effects for patients with IBS. Complementary therapies, such as acupuncture or abdominal massage, have received more attention in recent years. In this study, a rat model of IBS with diarrhea (IBS-D) was established by instillation of acetic acid from the colon. The effects of abdominal massage on changes in gut motility, visceral hypersensitivity, and the possible mechanism were investigated. Continuous abdominal massage could decrease the stool consistency score and increase the efflux time of glass beads compared with model groups, while also decreasing mast cell counts in IBS-D rats. The mRNA and protein expressions of neuronal nitric oxide synthase (nNOS), choline acetyl transferase (CHAT), and protein gene product 9.5 (PGP9.5) were significantly upregulated by continuous abdominal massage compared with model groups. Continuous abdominal massage also improved the ultrastructure of enteric glial cells (EGCs) by decreasing the number of mitochondria and increasing the level of the heterochromatin. Meanwhile, continuous abdominal massage could upregulate the expression of glial cell line-derived neurotrophic factor (GDNF) and P-Akt/Akt. Furthermore, it could reduce visceral hypersensitivity and improve the IBS-D symptoms by regulating the phosphoinositide 3-kinase (PI3K)-Akt pathway, which would provide a novel method for the treatment of IBS-D in the clinical setting.
Keyphrases
- irritable bowel syndrome
- signaling pathway
- nitric oxide synthase
- pi k akt
- cell proliferation
- drug induced
- insulin resistance
- cell cycle arrest
- nitric oxide
- induced apoptosis
- binding protein
- cell death
- type diabetes
- skeletal muscle
- transcription factor
- physical activity
- working memory
- genome wide
- mass spectrometry
- cystic fibrosis
- adipose tissue
- small molecule
- subarachnoid hemorrhage
- tyrosine kinase
- single molecule
- oxidative stress
- amino acid
- sleep quality
- smoking cessation
- brain injury
- atomic force microscopy
- endoplasmic reticulum
- electronic health record
- adverse drug