Title: M64HCl, a focal adhesion kinase activator, promotes intestinal mucosal healing in rats
Version: 0 Date: 02 Aug 2024
Reviewer's report:
In this manuscript, Guiming Liu and colleagues concluded that M64HCl, a water-soluble FAK
activator, promotes acetic acid-induced ulcer healing in rats. Some experiments were well
designed and performed. The text was written in a scientific and professional manner. However,
the data are not suitable for publication at this stage. Further experimental data are needed to
support the conclusions of this study.
1.It would be better to add images of acetic acid-induced intestinal ulcers to Figure1.
2.It would be better to add H&E staining to show the morphology of the bowel in both the normal
state and the acetic acid-induced ulcer before treatment in Figure 2.
3.It would be better to show the p-FAK IHC staining in both the normal condition and the acetic
acid-induced ulcer before treatment in Figure 3.
4.The authors should perform a thorough histopathological analysis of the tissues collected in
the acetic acid-induced ulcer experiments. Intestinal epithelial cell proliferation and apoptosis
assays are required to assess the effect of M64HCl on intestinal epithelial repair.
5.The level of inflammation and intestinal barrier permeability before and after M64HCl
treatment are also important indicators. HE staining alone is not sufficient, it would be better to
add serum IL-1#, TNF-# and other inflammatory factors to Figure 2.
6.The authors should quantitatively analyse p-KAK expression by Western blot in intestinal
tissues treated with M64HCl vs. controls.
7.When M64HCl enters an organism such as a mouse or rat, is there a metabolic change in its
molecular structure?
Title: M64HCl, a focal adhesion kinase activator, promotes intestinal mucosal healing in rats
Version: 0 Date: 02 Aug 2024
Reviewer's report:
In this manuscript, Guiming Liu and colleagues concluded that M64HCl, a water-soluble FAK
activator, promotes acetic acid-induced ulcer healing in rats. Some experiments were well
designed and performed. The text was written in a scientific and professional manner. However,
the data are not suitable for publication at this stage. Further experimental data are needed to
support the conclusions of this study.
1.It would be better to add images of acetic acid-induced intestinal ulcers to Figure1.
2.It would be better to add H&E staining to show the morphology of the bowel in both the normal
state and the acetic acid-induced ulcer before treatment in Figure 2.
3.It would be better to show the p-FAK IHC staining in both the normal condition and the acetic
acid-induced ulcer before treatment in Figure 3.
4.The authors should perform a thorough histopathological analysis of the tissues collected in
the acetic acid-induced ulcer experiments. Intestinal epithelial cell proliferation and apoptosis
assays are required to assess the effect of M64HCl on intestinal epithelial repair.
5.The level of inflammation and intestinal barrier permeability before and after M64HCl
treatment are also important indicators. HE staining alone is not sufficient, it would be better to
add serum IL-1#, TNF-# and other inflammatory factors to Figure 2.
6.The authors should quantitatively analyse p-KAK expression by Western blot in intestinal
tissues treated with M64HCl vs. controls.
7.When M64HCl enters an organism such as a mouse or rat, is there a metabolic change in its
molecular structure?
Please review this paper.
user
Title: M64HCl, a focal adhesion kinase activator, promotes intestinal mucosal healing in rats
Version: 0 Date: 02 Aug 2024
Reviewer's report:
In this manuscript, Guiming Liu and colleagues concluded that M64HCl, a water-soluble FAK
activator, promotes acetic acid-induced ulcer healing in rats. Some experiments were well
designed and performed. The text was written in a scientific and professional manner. However,
the data are not suitable for publication at this stage. Further experimental data are needed to
support the conclusions of this study.
1.It would be better to add images of acetic acid-induced intestinal ulcers to Figure1.
2.It would be better to add H&E staining to show the morphology of the bowel in both the normal
state and the acetic acid-induced ulcer before treatment in Figure 2.
3.It would be better to show the p-FAK IHC staining in both the normal condition and the acetic
acid-induced ulcer before treatment in Figure 3.
4.The authors should perform a thorough histopathological analysis of the tissues collected in
the acetic acid-induced ulcer experiments. Intestinal epithelial cell proliferation and apoptosis
assays are required to assess the effect of M64HCl on intestinal epithelial repair.
5.The level of inflammation and intestinal barrier permeability before and after M64HCl
treatment are also important indicators. HE staining alone is not sufficient, it would be better to
add serum IL-1#, TNF-# and other inflammatory factors to Figure 2.
6.The authors should quantitatively analyse p-KAK expression by Western blot in intestinal
tissues treated with M64HCl vs. controls.
7.When M64HCl enters an organism such as a mouse or rat, is there a metabolic change in its
molecular structure?
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