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Ophiopogon japonicas (Linn. f.) Ker-Gawl. extract ameliorates chronic heart failure in rats
Author(s) -
Hu-zhi Cai,
Yanping Tang,
Xinyu Chen,
Xie HaiBo,
Qingyang Chen,
Zelin Xu
Publication year - 2021
Publication title -
tropical journal of pharmaceutical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.209
H-Index - 36
eISSN - 1596-5996
pISSN - 1596-9827
DOI - 10.4314/tjpr.v18i9.10
Subject(s) - malondialdehyde , captopril , heart failure , preload , hemodynamics , medicine , blood pressure , ventricular pressure , nitric oxide , heart rate , cardiology , endocrinology , oxidative stress
Purpose: To investigate the effect of Ophiopogon japonicas (Linn. f.) Ker-Gawl. extract (OJKE) on oxidative stress and hemodynamics in chronic congestive heart failure (CHF) rats. Methods: The rats were modelled to congestive heart failure (except normal group) , and then randomly divided into normal control group, model (untreated) group, captopril group, high-dose, middle-dose and low-dose of OJKE groups. They were treated for 4 weeks as appropriate for each group. At the end of treatment, the hemodynamic function, whole heart weight index, and blood creatinine kinase (CK), as well as superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), nitricoxide synthase (NOS) were determined. Results: Compared with the normal control group, arterial systolic pressure (SBP), diastolic pressure (DBP), mean arterial pressure (MAP), heart rate (HR), left ventricular systolic peak (LVSP), and left ventricular pressure change rate (dp/dt max) significantly decreased (p < 0.05), while left ventricular end diastolic pressure (LVEDP), whole heart weight index, blood CK, MDA, NO, NOS significantly increased in the untreated group (p < 0.05). A high dose of OJKE significantly improved hemodynamic function, lowered MDA (8.33 ± 2.12 nmol/mL) and NO (20.58 ± 3.53 umol/L) levels (p < 0.05), and also decreased CK (0.53±0.37 U/mL) and NOS (22.46±3.29 U/mL) in CHF rats (p < 0.05). Conclusion: OJKE improved adriamycin-induced chronic congestive heart failure in rats significantly.

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