Mei, C.
Resveratrol inhibits myocardial apoptosis by regulating the protein kinase r-like endoplasmic reticulum kinase endoplasmic reticulum stress pathway and improves myocardial remodeling and cardiac function after myocardial infarction - Vol.83(2), March-April - Mumbai Indian Journal of Pharmaceutical Science 2021 - 387-392p.
To analyze the e ffect of resveratrol on myocardial remodeling and cardiac function after myocardial
infarction by inhibiting myocardial cell apoptosis through regulating silent information regulator 1/protein
kinase R-like endoplasmic reticulum kinase pathway. 32 healthy male sprague dawley rats were divided
into control group (without any treatment), model group (ligation of left anterior descending branch to
establish a model), sham operation group (ligation of left anterior descending branch without ligation)
and resveratrol group (ligation of left anterior descending branch+resveratrol 8 mg/kg/d), 8 rats each.
The changes of cardiac function, myocardial remodeling, myocardial apoptosis and silent information
regulator 1/protein kinase R-like endoplasmic reticulum kinase pathway related proteins were observed
4 w after modeling. Left ventricular end-diastolic diameter and left ventricular end-systolic dimension
levels in the model group were significantly higher than those in the control group, left ventricular ejection
fraction and left ventricular short axis shortening rate levels were signi ficantly lower than those in the
control group (p<0.01), left ventricular end-diastolic diameter and left ventricular end-systolic dimension
levels in the resveratrol group were significantly lower than those in the model group and left ventricular
ejection fraction and left ventricular short axis shortening rate levels were signi ficantly higher than those
in the model group (p<0.01). In the model group, the myocardial cells were arranged in a disordered
manner and fibrogenic hyperplasia occurred, while the pathological changes of the myocardial cells in
the resveratrol group were reduced compared with the model group. The collagen volume fraction of
myocardial tissue in the model group was significantly higher than that in the control group (p<0.05) and
the collagen volume fraction in the resveratrol group was significantly lower than that in the model group
(p<0.05). The apoptosis rate of myocardial cells in the model group was significantly higher than that in the
control group (p<0.01) and the apoptosis rate of myocardial cells in the resveratrol group was significantly
lower than that in the model group (p<0.01). The expression levels of Phosphate-protein kinase R like
endoplasmic reticulum kinase, Phosphate eukaryotic initiation factor 2 and Activating transcription factor
4 in the model group were signi ficantly higher than those of the control group and the expression levels
of Silent Information Regulator 1 were signi ficantly lower than those of the control group (p<0.01). The
expression levels of Phosphate-protein kinase R like endoplasmic reticulum kinase, Phosphate eukaryotic
initiation factor 2 and Activating transcription factor 4 in the resveratrol group were signi ficantly lower
than those of the model group and the expression levels of silent information regulator 1 were significantly
higher than those of the model group (p<0.01). Resveratrol can reduce apoptosis of myocardial cells after
myocardial infarction by regulating the silent information regulator 1/protein kinase R-like endoplasmic
reticulum kinase pathway endoplasmic reticulum stress pathway and improve myocardial remodeling and
cardiac function in rats, providing a new target for clinical treatment of myocardial infarction.
PHARMACEUTICS
Resveratrol inhibits myocardial apoptosis by regulating the protein kinase r-like endoplasmic reticulum kinase endoplasmic reticulum stress pathway and improves myocardial remodeling and cardiac function after myocardial infarction - Vol.83(2), March-April - Mumbai Indian Journal of Pharmaceutical Science 2021 - 387-392p.
To analyze the e ffect of resveratrol on myocardial remodeling and cardiac function after myocardial
infarction by inhibiting myocardial cell apoptosis through regulating silent information regulator 1/protein
kinase R-like endoplasmic reticulum kinase pathway. 32 healthy male sprague dawley rats were divided
into control group (without any treatment), model group (ligation of left anterior descending branch to
establish a model), sham operation group (ligation of left anterior descending branch without ligation)
and resveratrol group (ligation of left anterior descending branch+resveratrol 8 mg/kg/d), 8 rats each.
The changes of cardiac function, myocardial remodeling, myocardial apoptosis and silent information
regulator 1/protein kinase R-like endoplasmic reticulum kinase pathway related proteins were observed
4 w after modeling. Left ventricular end-diastolic diameter and left ventricular end-systolic dimension
levels in the model group were significantly higher than those in the control group, left ventricular ejection
fraction and left ventricular short axis shortening rate levels were signi ficantly lower than those in the
control group (p<0.01), left ventricular end-diastolic diameter and left ventricular end-systolic dimension
levels in the resveratrol group were significantly lower than those in the model group and left ventricular
ejection fraction and left ventricular short axis shortening rate levels were signi ficantly higher than those
in the model group (p<0.01). In the model group, the myocardial cells were arranged in a disordered
manner and fibrogenic hyperplasia occurred, while the pathological changes of the myocardial cells in
the resveratrol group were reduced compared with the model group. The collagen volume fraction of
myocardial tissue in the model group was significantly higher than that in the control group (p<0.05) and
the collagen volume fraction in the resveratrol group was significantly lower than that in the model group
(p<0.05). The apoptosis rate of myocardial cells in the model group was significantly higher than that in the
control group (p<0.01) and the apoptosis rate of myocardial cells in the resveratrol group was significantly
lower than that in the model group (p<0.01). The expression levels of Phosphate-protein kinase R like
endoplasmic reticulum kinase, Phosphate eukaryotic initiation factor 2 and Activating transcription factor
4 in the model group were signi ficantly higher than those of the control group and the expression levels
of Silent Information Regulator 1 were signi ficantly lower than those of the control group (p<0.01). The
expression levels of Phosphate-protein kinase R like endoplasmic reticulum kinase, Phosphate eukaryotic
initiation factor 2 and Activating transcription factor 4 in the resveratrol group were signi ficantly lower
than those of the model group and the expression levels of silent information regulator 1 were significantly
higher than those of the model group (p<0.01). Resveratrol can reduce apoptosis of myocardial cells after
myocardial infarction by regulating the silent information regulator 1/protein kinase R-like endoplasmic
reticulum kinase pathway endoplasmic reticulum stress pathway and improve myocardial remodeling and
cardiac function in rats, providing a new target for clinical treatment of myocardial infarction.
PHARMACEUTICS