Beneficial effects of andrographolide in a rat model of autoimmune myocarditis and its effects on PI3K/Akt pathway
The Korean Journal of Physiology and Pharmacology
; : 103-111, 2019.
Article
in En
| WPRIM
| ID: wpr-728018
Responsible library:
WPRO
ABSTRACT
The study is to investigate effects of andrographolide on experimental autoimmune myocarditis (EAM). Lewis rats were immunized on day 0 with porcine cardiac myosin to establish EAM. The EAM rats were treated with either andrographolide (25, 50, 100 mg/kg/day) or vehicle for 21 days. An antigen-specific splenocytes proliferation assay was performed by using the cells from control rats immunized with cardiac myosin. Survival rates, myocardial pathology and myocardial functional parameters (left ventricle end-diastolic pressure, ± dP/dt and left ventricular internal dimension) of EAM rats received andrographolide were significantly improved. Andrographolide treatment caused an decrease in the infiltration of CD3⁺ and CD14⁺ positive cells in myocardial tissue. Moreover, andrographolide treatment caused a reduction in the plasma levels of tumor necrosis factor-alpha, interleukin-17 (IL-17) and myosin-antibody, and an increase in the level of IL-10 in EAM rats. Oral administration of andrographolide resulted in the decreased expression of p-PI3K, p-Akt without any change of PI3K and Akt. Further results indicate andrographolide significantly inhibited myosin-induced proliferation in splenocytes, and this effect was inhibited by co-treatment of SC79 (Akt activator). Our data indicate andrographolide inhibits development of EAM, and this beneficial effect may be due to powerful anti-inflammatory activity and inhibitory effect on PI3K/Akt pathway.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Pathology
/
Plasma
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Administration, Oral
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Survival Rate
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Tumor Necrosis Factor-alpha
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Interleukin-10
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Interleukin-17
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Models, Animal
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Cardiac Myosins
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Myocarditis
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2019
Type:
Article