Title: Vitamin B6 ameliorates acute pancreatitis by suppressing the Caspase3 signaling pathway
Version: 7 Date: 21 Feb 2024
Reviewer:  Li-Kang Sun
Reviewer's report:
To the revised manuscript, which entitled “Vitamin B6 ameliorates acute pancreatitis by
suppressing the Caspase3 signalling pathway”, Authors tried to improve the manuscript, and
effective change a lot. It makes me difficult to make a decision. So I would like use this
opportunity to discuss the questions which I mentioned before again:
First at all, the major point, acute pancreatitis was defined as an inflammatory disease, the
pathological change were focused on inflammation and necrosis; the characteristic changes of
taurocholate sodium induced pancreatitis model were inflammation and necrosis, too.
Per definitions, necrosis and apoptosis are different patho-physiological processes, somehow,
necrosis is generally characterized to be the uncontrolled death of the cell, usually following
a severe insult, resulting in spillage of the contents of the cell into surrounding tissues and
subsequent then caused the inflammation, and the process of apoptosis is characterized by
a number of characteristic morphological changes in the structure of the cell, together with
a number of enzyme-dependent biochemical processes. The result being the clearance of
cells from the body, with minimal damage to surrounding tissues, which do not correlated to
inflammation.
The authors presented experiments demonstrated that, in the in vivo experiment, both necrosis
and apoptosis are co-exist. The Authors emphasized “Vitamin B6 ameliorates acute pancreatitis
by suppressing the Caspase3 signalling pathway”. So that more depth discussion are required to
augment why Authors ignore the necrosis changes and emphasize the apoptosis changes.
Second, be sure, AR42J cell in vitro experiment cannot be defined as “Cell AP model”, perhaps
could be defined as an acinar inflammation experiment. The number of experiments or samples
in the statistical analysis should mentioned. Overall of pathological staining the bar-scale should
present.
Third, not really the minor point, the different linguistic problems, spelling errors and spelling
problems are still present, please check carefully before resubmission, or Authors ask for
professional help. Definitely, the manual editing of literature reference could cause big trouble
by publication process.
Title: Vitamin B6 ameliorates acute pancreatitis by suppressing the Caspase3 signaling pathway
Version: 7 Date: 21 Feb 2024
Reviewer:  Li-Kang Sun
Reviewer's report:
To the revised manuscript, which entitled “Vitamin B6 ameliorates acute pancreatitis by
suppressing the Caspase3 signalling pathway”, Authors tried to improve the manuscript, and
effective change a lot. It makes me difficult to make a decision. So I would like use this
opportunity to discuss the questions which I mentioned before again:
First at all, the major point, acute pancreatitis was defined as an inflammatory disease, the
pathological change were focused on inflammation and necrosis; the characteristic changes of
taurocholate sodium induced pancreatitis model were inflammation and necrosis, too.
Per definitions, necrosis and apoptosis are different patho-physiological processes, somehow,
necrosis is generally characterized to be the uncontrolled death of the cell, usually following
a severe insult, resulting in spillage of the contents of the cell into surrounding tissues and
subsequent then caused the inflammation, and the process of apoptosis is characterized by
a number of characteristic morphological changes in the structure of the cell, together with
a number of enzyme-dependent biochemical processes. The result being the clearance of
cells from the body, with minimal damage to surrounding tissues, which do not correlated to
inflammation.
The authors presented experiments demonstrated that, in the in vivo experiment, both necrosis
and apoptosis are co-exist. The Authors emphasized “Vitamin B6 ameliorates acute pancreatitis
by suppressing the Caspase3 signalling pathway”. So that more depth discussion are required to
augment why Authors ignore the necrosis changes and emphasize the apoptosis changes.
Second, be sure, AR42J cell in vitro experiment cannot be defined as “Cell AP model”, perhaps
could be defined as an acinar inflammation experiment. The number of experiments or samples
in the statistical analysis should mentioned. Overall of pathological staining the bar-scale should
present.
Third, not really the minor point, the different linguistic problems, spelling errors and spelling
problems are still present, please check carefully before resubmission, or Authors ask for
professional help. Definitely, the manual editing of literature reference could cause big trouble
by publication process.
Please review this paper.
user
Title: Vitamin B6 ameliorates acute pancreatitis by suppressing the Caspase3 signaling pathway
Version: 7 Date: 21 Feb 2024
Reviewer:  Li-Kang Sun
Reviewer's report:
To the revised manuscript, which entitled “Vitamin B6 ameliorates acute pancreatitis by
suppressing the Caspase3 signalling pathway”, Authors tried to improve the manuscript, and
effective change a lot. It makes me difficult to make a decision. So I would like use this
opportunity to discuss the questions which I mentioned before again:
First at all, the major point, acute pancreatitis was defined as an inflammatory disease, the
pathological change were focused on inflammation and necrosis; the characteristic changes of
taurocholate sodium induced pancreatitis model were inflammation and necrosis, too.
Per definitions, necrosis and apoptosis are different patho-physiological processes, somehow,
necrosis is generally characterized to be the uncontrolled death of the cell, usually following
a severe insult, resulting in spillage of the contents of the cell into surrounding tissues and
subsequent then caused the inflammation, and the process of apoptosis is characterized by
a number of characteristic morphological changes in the structure of the cell, together with
a number of enzyme-dependent biochemical processes. The result being the clearance of
cells from the body, with minimal damage to surrounding tissues, which do not correlated to
inflammation.
The authors presented experiments demonstrated that, in the in vivo experiment, both necrosis
and apoptosis are co-exist. The Authors emphasized “Vitamin B6 ameliorates acute pancreatitis
by suppressing the Caspase3 signalling pathway”. So that more depth discussion are required to
augment why Authors ignore the necrosis changes and emphasize the apoptosis changes.
Second, be sure, AR42J cell in vitro experiment cannot be defined as “Cell AP model”, perhaps
could be defined as an acinar inflammation experiment. The number of experiments or samples
in the statistical analysis should mentioned. Overall of pathological staining the bar-scale should
present.
Third, not really the minor point, the different linguistic problems, spelling errors and spelling
problems are still present, please check carefully before resubmission, or Authors ask for
professional help. Definitely, the manual editing of literature reference could cause big trouble
by publication process.
assistant