APMCG-1 improves cardiomyocytes in larvae
To validate whether APMCG-1 normalizes cardiomyocytes and skeletal
myoblasts capacities, we analyzed the functional and energy metabolism
in of type 2 diabetic zebrafish model. The heart rate of zebrafish
refers to the heart beats per minute, and the change in heart rate is an
important index for the evaluation of cardiac function. Compared with
that of the untreated group, the heart rate of zebrafish in the model
group decreased, and the mortality increased. Compared with the model
group, different concentrations of APMCG-1 increased the heart rate and
decreased mortality (Fig. 4A, 4B). After five days of continuous
high-cholesterol feeding, accumulation of lipid deposition was observed
at the bifurcation of blood vessels, which indicated that high blood
lipid levels can promote and cause the occurrence of atherosclerosis and
lead to the localization of atherosclerosis (Fig. 4C). The blood flow
rate of larvae in the model group was significantly decreased, and the
decreased blood flow rate was significantly recovered after 50 μg/mL
APMCG-1 treatment (Fig. 4D). Therefore, 50 μg/mL APMCG-1 was selected
for follow-up experiments.
Insulin resistance is an independent risk factor for diabetes. Compared
with the model group, the increased concentrations of APMCG-1 decreased
the levels of FBG, T-CHO, and TG dose-dependently in the treated group.
This finding illustrates that APMCG-1 regulated blood glucose and lipid
levels in type 2 diabetic zebrafish. CK-MB is a subtype of CK that is
found only in the heart and cTnI is a specific marker of myocardial
necrosis. Thus, CK-MB and cTnI are associated with myocardial injury. We
observed that APMCG-1 markedly decreased the levels of CK-MB and cTnI
compared with those in the model zebrafish, which revealed that APMCG-1
can reduce cardiac injury (Fig. 4E). Compared with the model group,
APMCG-1 significantly increased the levels of SOD, GSH-PX and CAT, and
decreased the level of MDA, TNF-ɑ and IL-6 in the treatment group (Fig.
4F). Collectively, the data suggested that APMCG-1 predominately
promotes glucose uptake and metabolism in cardiomyocytes and skeletal
myoblasts.