Title: Sodium nitroprusside protects HFD induced gut dysfunction via activating AMPK#/
SIRT1 signaling
Version: 2 Date: 22 Dec 2020
Reviewer's report:
In this study, the authors have investigated the potential mitigating effects of the NO donor,
sodium nitroprusside (SNP). Using the Caco-2 cells, they show that LPS reduces the expression
of tight junction proteins, which is reversed by SNP treatment. Using the high-fat diet-fed mouse
model, they show that SNP reverses some of HFD feeding effects. The results appear to be
interesting, and the study is mechanistic. However, there are numerous issues in the study design
and presentation, including a lack of crucial control groups.
Major
1. Fig 1: Perform densitometric analysis and present data in graphs with statistical analysis. Are
there effects of LPS and SNP associated with similar changes in the epithelial permeability?
2. Fig. 1C&D: This study needs to include NC-siRNA and siAMPK controls.
3. Fig 2: The study needs an SNP control group.
4. Fig. 2: The data show that the bodyweight increased by HFD in almost entirely reversed
by SNP. However, the fat mass increase is reversed only partially. The data presented is the
total fat mass, which means the fat per g body weight is even higher. This discrepancy begs the
question of what is the cause of reduced body weight? The caption of this figure in the legend
is, therefore, misleading.
5. Fig 3H: the magnification of the HFD group is taken from the half of the section that seems
to be affected while the other half of the section appears normal. Is this consistent with sections
from other animals, or is it a sectioning artifact?
6. The HFD+SNP intestine appears to have many goblet cells. An explanation of this observation
requires it is to include an SNP control group.
Minor
1. Figure legend: please describe the experimental setup rather than summarizing the results.
2. There are too many typos and grammatical errors. The manuscript needs to be professionally
checked for English.
Title: Sodium nitroprusside protects HFD induced gut dysfunction via activating AMPK#/
SIRT1 signaling
Version: 2 Date: 22 Dec 2020
Reviewer's report:
In this study, the authors have investigated the potential mitigating effects of the NO donor,
sodium nitroprusside (SNP). Using the Caco-2 cells, they show that LPS reduces the expression
of tight junction proteins, which is reversed by SNP treatment. Using the high-fat diet-fed mouse
model, they show that SNP reverses some of HFD feeding effects. The results appear to be
interesting, and the study is mechanistic. However, there are numerous issues in the study design
and presentation, including a lack of crucial control groups.
Major
1. Fig 1: Perform densitometric analysis and present data in graphs with statistical analysis. Are
there effects of LPS and SNP associated with similar changes in the epithelial permeability?
2. Fig. 1C&D: This study needs to include NC-siRNA and siAMPK controls.
3. Fig 2: The study needs an SNP control group.
4. Fig. 2: The data show that the bodyweight increased by HFD in almost entirely reversed
by SNP. However, the fat mass increase is reversed only partially. The data presented is the
total fat mass, which means the fat per g body weight is even higher. This discrepancy begs the
question of what is the cause of reduced body weight? The caption of this figure in the legend
is, therefore, misleading.
5. Fig 3H: the magnification of the HFD group is taken from the half of the section that seems
to be affected while the other half of the section appears normal. Is this consistent with sections
from other animals, or is it a sectioning artifact?
6. The HFD+SNP intestine appears to have many goblet cells. An explanation of this observation
requires it is to include an SNP control group.
Minor
1. Figure legend: please describe the experimental setup rather than summarizing the results.
2. There are too many typos and grammatical errors. The manuscript needs to be professionally
checked for English.
Please review this paper.
user
Title: Sodium nitroprusside protects HFD induced gut dysfunction via activating AMPK#/
SIRT1 signaling
Version: 2 Date: 22 Dec 2020
Reviewer's report:
In this study, the authors have investigated the potential mitigating effects of the NO donor,
sodium nitroprusside (SNP). Using the Caco-2 cells, they show that LPS reduces the expression
of tight junction proteins, which is reversed by SNP treatment. Using the high-fat diet-fed mouse
model, they show that SNP reverses some of HFD feeding effects. The results appear to be
interesting, and the study is mechanistic. However, there are numerous issues in the study design
and presentation, including a lack of crucial control groups.
Major
1. Fig 1: Perform densitometric analysis and present data in graphs with statistical analysis. Are
there effects of LPS and SNP associated with similar changes in the epithelial permeability?
2. Fig. 1C&D: This study needs to include NC-siRNA and siAMPK controls.
3. Fig 2: The study needs an SNP control group.
4. Fig. 2: The data show that the bodyweight increased by HFD in almost entirely reversed
by SNP. However, the fat mass increase is reversed only partially. The data presented is the
total fat mass, which means the fat per g body weight is even higher. This discrepancy begs the
question of what is the cause of reduced body weight? The caption of this figure in the legend
is, therefore, misleading.
5. Fig 3H: the magnification of the HFD group is taken from the half of the section that seems
to be affected while the other half of the section appears normal. Is this consistent with sections
from other animals, or is it a sectioning artifact?
6. The HFD+SNP intestine appears to have many goblet cells. An explanation of this observation
requires it is to include an SNP control group.
Minor
1. Figure legend: please describe the experimental setup rather than summarizing the results.
2. There are too many typos and grammatical errors. The manuscript needs to be professionally
checked for English.
assistant