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β-Caryophyllene as a Potential Protective Agent Against Myocardial Injury: The Role of Toll-Like Receptors.
Molecules 2019; 24(10)M

Abstract

Myocardial infarction (MI) remains one of the major causes of mortality around the world. A possible mechanism involved in myocardial infarction is the engagement of Toll-like receptors (TLRs). This study was intended to discover the prospective cardioprotective actions of β-caryophyllene, a natural sesquiterpene, to ameliorate isoproterenol (ISO)-induced myocardial infarction through HSP-60/TLR/MyD88/NFκB pathway. β-Caryophyllene (100 or 200 mg/kg/day orally) was administered for 21 days then MI was induced via ISO (85 mg/kg, subcutaneous) on 20th and 21st days. The results indicated that ISO induced a significant infarcted area associated with several alterations in the electrocardiogram (ECG) and blood pressure (BP) indices and caused an increase in numerous cardiac indicators such as creatine phosphokinase (CPK), creatine kinase-myocardial bound (CK-MB), lactate dehydrogenase (LDH), and cardiac tropinine T (cTnT). In addition, ISO significantly amplified heat shock protein 60 (HSP-60) and other inflammatory markers, such as TNF-α, IL-Iβ, and NFκB, and affected TLR2 and TLR4 expression and their adaptor proteins; Myeloid differentiation primary response 88 (MYD88), and TIR-domain-containing adapter-inducing interferon-β (TRIF). On the other hand, consumption of β-caryophyllene significantly reversed the infarcted size, ECG and BP alterations, ameliorated the ISO elevation in cardiac indicators; it also notably diminished HSP-60, and subsequently TLR2, TLR4, MYD88, and TRIF expression, with a substantial reduction in inflammatory mediator levels. This study revealed the cardioprotective effect of β-caryophyllene against MI through inhibiting HSP-60/TLR/MyD88/NFκB signaling pathways.

Authors+Show Affiliations

Department of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, 31982 Al-Ahsa, Saudi Arabia. nyounis@kfu.edu.sa. Department of Pharmacology, Zagazig University, Zagazig 44519, Egypt. nyounis@kfu.edu.sa.Department of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, 31982 Al-Ahsa, Saudi Arabia. MAGED789@HOTMAIL.COM. Department of Pharmacognosy, College of Pharmacy, Zagazig University, Zagazig 44519, Egypt. MAGED789@HOTMAIL.COM.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31109132

Citation

Younis, Nancy S., and Maged E. Mohamed. "Β-Caryophyllene as a Potential Protective Agent Against Myocardial Injury: the Role of Toll-Like Receptors." Molecules (Basel, Switzerland), vol. 24, no. 10, 2019.
Younis NS, Mohamed ME. Β-Caryophyllene as a Potential Protective Agent Against Myocardial Injury: The Role of Toll-Like Receptors. Molecules. 2019;24(10).
Younis, N. S., & Mohamed, M. E. (2019). Β-Caryophyllene as a Potential Protective Agent Against Myocardial Injury: The Role of Toll-Like Receptors. Molecules (Basel, Switzerland), 24(10), doi:10.3390/molecules24101929.
Younis NS, Mohamed ME. Β-Caryophyllene as a Potential Protective Agent Against Myocardial Injury: the Role of Toll-Like Receptors. Molecules. 2019 May 19;24(10) PubMed PMID: 31109132.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - β-Caryophyllene as a Potential Protective Agent Against Myocardial Injury: The Role of Toll-Like Receptors. AU - Younis,Nancy S, AU - Mohamed,Maged E, Y1 - 2019/05/19/ PY - 2019/04/12/received PY - 2019/05/10/revised PY - 2019/05/16/accepted PY - 2019/5/22/entrez PY - 2019/5/22/pubmed PY - 2019/5/22/medline KW - MyD88 KW - heat shock protein 60 KW - isoproterenol KW - toll-like receptors KW - β-caryophyllene JF - Molecules (Basel, Switzerland) JO - Molecules VL - 24 IS - 10 N2 - Myocardial infarction (MI) remains one of the major causes of mortality around the world. A possible mechanism involved in myocardial infarction is the engagement of Toll-like receptors (TLRs). This study was intended to discover the prospective cardioprotective actions of β-caryophyllene, a natural sesquiterpene, to ameliorate isoproterenol (ISO)-induced myocardial infarction through HSP-60/TLR/MyD88/NFκB pathway. β-Caryophyllene (100 or 200 mg/kg/day orally) was administered for 21 days then MI was induced via ISO (85 mg/kg, subcutaneous) on 20th and 21st days. The results indicated that ISO induced a significant infarcted area associated with several alterations in the electrocardiogram (ECG) and blood pressure (BP) indices and caused an increase in numerous cardiac indicators such as creatine phosphokinase (CPK), creatine kinase-myocardial bound (CK-MB), lactate dehydrogenase (LDH), and cardiac tropinine T (cTnT). In addition, ISO significantly amplified heat shock protein 60 (HSP-60) and other inflammatory markers, such as TNF-α, IL-Iβ, and NFκB, and affected TLR2 and TLR4 expression and their adaptor proteins; Myeloid differentiation primary response 88 (MYD88), and TIR-domain-containing adapter-inducing interferon-β (TRIF). On the other hand, consumption of β-caryophyllene significantly reversed the infarcted size, ECG and BP alterations, ameliorated the ISO elevation in cardiac indicators; it also notably diminished HSP-60, and subsequently TLR2, TLR4, MYD88, and TRIF expression, with a substantial reduction in inflammatory mediator levels. This study revealed the cardioprotective effect of β-caryophyllene against MI through inhibiting HSP-60/TLR/MyD88/NFκB signaling pathways. SN - 1420-3049 UR - https://www.unboundmedicine.com/medline/citation/31109132/β-Caryophyllene_as_a_Potential_Protective_Agent_Against_Myocardial_Injury:_The_Role_of_Toll-Like_Receptors L2 - http://www.mdpi.com/resolver?pii=molecules24101929 DB - PRIME DP - Unbound Medicine ER -
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