Title: M64HCl, a focal adhesion kinase activator, promotes intestinal mucosal healing in rats
Version: 0 Date: 02 Aug 2024
Reviewer's report:
I do not support the publication of this manuscript. In this article, the authors aim to identify
if M64HCl treatment in rats with intestinal injury (induced by 75% acetic acid) can promote
intestinal healing (effects that are observed in mice). Here, the authors claim to observe an
improvement in ulcer area, pFAK immunoreactivity and alleviation of intestinal pathology.
First, we do not know the extent to which intestinal injury is established in the basic model
in the rats, as this has not been described sufficiently especially in this rat model (i.e., clinical
scoring signs, cytokine profiles, weight change, survival, etc.). The authors refer to “pathological
factors” as causes for mucosal injury but no pathogens were tested thus overstating the relevance
of their findings. The data presented by the authors is also very weak and does not accurately
represent what the authors are claiming to be true. Although the authors show that there is a
reduction in ulcer area in figure 1 (where C and D are repeats), the evidence for improvement
in intestinal pathology and FAK activation is limited (H&E and immunohistochemistry do not
capture what the authors claim to be the case -> the images are very weak, staining issues, etc.).
For example, the authors claim things like increased inflammatory cells but the provided images
do not capture this. These 3 figures plus a table are the only results provided but this is very
weak evidence.
Title: M64HCl, a focal adhesion kinase activator, promotes intestinal mucosal healing in rats
Version: 0 Date: 02 Aug 2024
Reviewer's report:
I do not support the publication of this manuscript. In this article, the authors aim to identify
if M64HCl treatment in rats with intestinal injury (induced by 75% acetic acid) can promote
intestinal healing (effects that are observed in mice). Here, the authors claim to observe an
improvement in ulcer area, pFAK immunoreactivity and alleviation of intestinal pathology.
First, we do not know the extent to which intestinal injury is established in the basic model
in the rats, as this has not been described sufficiently especially in this rat model (i.e., clinical
scoring signs, cytokine profiles, weight change, survival, etc.). The authors refer to “pathological
factors” as causes for mucosal injury but no pathogens were tested thus overstating the relevance
of their findings. The data presented by the authors is also very weak and does not accurately
represent what the authors are claiming to be true. Although the authors show that there is a
reduction in ulcer area in figure 1 (where C and D are repeats), the evidence for improvement
in intestinal pathology and FAK activation is limited (H&E and immunohistochemistry do not
capture what the authors claim to be the case -> the images are very weak, staining issues, etc.).
For example, the authors claim things like increased inflammatory cells but the provided images
do not capture this. These 3 figures plus a table are the only results provided but this is very
weak evidence.
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:
I do not support the publication of this manuscript. In this article, the authors aim to identify
if M64HCl treatment in rats with intestinal injury (induced by 75% acetic acid) can promote
intestinal healing (effects that are observed in mice). Here, the authors claim to observe an
improvement in ulcer area, pFAK immunoreactivity and alleviation of intestinal pathology.
First, we do not know the extent to which intestinal injury is established in the basic model
in the rats, as this has not been described sufficiently especially in this rat model (i.e., clinical
scoring signs, cytokine profiles, weight change, survival, etc.). The authors refer to “pathological
factors” as causes for mucosal injury but no pathogens were tested thus overstating the relevance
of their findings. The data presented by the authors is also very weak and does not accurately
represent what the authors are claiming to be true. Although the authors show that there is a
reduction in ulcer area in figure 1 (where C and D are repeats), the evidence for improvement
in intestinal pathology and FAK activation is limited (H&E and immunohistochemistry do not
capture what the authors claim to be the case -> the images are very weak, staining issues, etc.).
For example, the authors claim things like increased inflammatory cells but the provided images
do not capture this. These 3 figures plus a table are the only results provided but this is very
weak evidence.
assistant