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Title: Ophiopogonin D alleviates cardiac hypertrophy in rat by upregulating CYP2J3 in vitro and suppressing inflammation in vivo

Journal Article · · Biochemical and Biophysical Research Communications
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  1. Department of Pharmacology and Toxicology, Institute of Radiation Medicine, Academy of Military Medical Sciences, Beijing 100850 (China)
  2. Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases (China)

Highlights: • OPD mostly exerts a positive effect on inhibiting pathological indexes in hypertrophy process. • Maybe the mechanism is decreasing the expression of NF-κB to suppress inflammation. • OPD overexpress the CYP2J3, which benefit the anti-inflammatory efficiency. Ophiopogonin D (OPD) is the chief pharmacological active component of the traditional Chinese herbal prescription drug-Shenmai injection (SMI), which has been used to prevent and treat cardiovascular diseases. In the present study, we investigated whether OPD protectively relieve cardiac hypertrophy against inflammation via inhibiting the expression of NF-κB and examined whether cytochrome P450 2J3 (CYP2J3)was involved in this pathway. H9c2 cells were treated with Angiotensin II (Ang II). Hypertrophy in rat was induced by administration of Ang II infusion. To evaluate the effect of OPD on disease progression and the role of CYP2J3 in this way, inflammatory mediators (NF-κB), specific hypertrophic factors and pathological change were determined in this experiment. Ang II induced hypertrophy with the elevated expression of specific hypertrophy genes and NF-κB signaling molecules. However, these inductive effects were reversed by OPD in conjunction with Ang II. Overexpression of CYP2J3 prevented the excessive expression of NF-κB. In vivo, partial pathological cardiac hypertrophy injuries were relieved after OPD treatment. OPD exerts a positive effect on alleviating cardiac hypertrophy. The mechanism is probably through inhibiting the expression of NF-κB by upregulating CYP2J3 to suppress inflammation.

OSTI ID:
23105612
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 503, Issue 2; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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