Hesham M Hassan, Muhammad Faisal Hayat, Ali Akbar, Azka Zafar, Khalid J Alzahrani, Fuad M Alzahrani, Abrar Aljohani
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Our findings revealed that EPH exposure provoked the gene expression of renin (REN), angiotensinogen (AGT), angiotensin I (Ang I), angiotensin II (Ang II), angiotensin II receptor type 1 (AGTR1), aldosterone synthase (CYP11B2), and mineralocorticoid receptor (NR3C2). The enzymatic activities of heme-oxygenase-1 (HO-1), glutathione peroxidase (GPx) (54.30 %), superoxide dismutase (SOD) (62.38 %), glutathione reductase (GSR) (54.80 %), catalase (CAT) (67.54 %), glutathione (GSH) (62.14 %) and glutathione S-transferase (GST) (44.25 %) were suppressed while the concentrations of reactive oxygen species (ROS) (2518.52 %) and malondialdehyde (MDA) (2654.55 %) were provoked after EPH intoxication. Besides, the EPH exposure exacerbated the concentration of N-terminal pro-B-type natriuretic peptide (ProBNP) (179.39), creatine kinase-myocardial band (CK-MB) (133.55 %), creatine phosphokinase (CPK) (180.72 %), C-reactive protein (CRP) (348.34 %), troponin-T (TnT) (1210.91 %), lactate dehydrogenase (LDH) (518.47 %), troponin-I (TnI) (1266.67 %) and brain natriuretic peptide (BNP) (243.34 %). The expression of Bax, and Caspase-3 were augmented while the expression of Bcl-2 was diminished after EPH administration. Moreover, EPH escalates the levels of interleukin-1beta (IL-1β) (471.71 %), cyclooxygenase-2 (COX-2) (304.16 %), tumor necrosis factor-alpha (TNF-α) (219.96 %), interleukin-6 (IL-6) (316.76 %), and nuclear factor-kappa B (NF-κB) (343.59 %) as well as significantly (p < 0.05) dysregulated the normal histology of cardiac tissues. Nevertheless, CAS treatment notably alleviated EPH instigated sub-chronic cardiac damage through the regulation of RAAS, oxidative stress, apoptosis, and inflammation. 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The enzymatic activities of heme-oxygenase-1 (HO-1), glutathione peroxidase (GPx) (54.30 %), superoxide dismutase (SOD) (62.38 %), glutathione reductase (GSR) (54.80 %), catalase (CAT) (67.54 %), glutathione (GSH) (62.14 %) and glutathione S-transferase (GST) (44.25 %) were suppressed while the concentrations of reactive oxygen species (ROS) (2518.52 %) and malondialdehyde (MDA) (2654.55 %) were provoked after EPH intoxication. Besides, the EPH exposure exacerbated the concentration of N-terminal pro-B-type natriuretic peptide (ProBNP) (179.39), creatine kinase-myocardial band (CK-MB) (133.55 %), creatine phosphokinase (CPK) (180.72 %), C-reactive protein (CRP) (348.34 %), troponin-T (TnT) (1210.91 %), lactate dehydrogenase (LDH) (518.47 %), troponin-I (TnI) (1266.67 %) and brain natriuretic peptide (BNP) (243.34 %). The expression of Bax, and Caspase-3 were augmented while the expression of Bcl-2 was diminished after EPH administration. 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Casuarinin modulates renin-angiotensin-aldosterone system to counter ephedrine-induced myocardial damage in rats.
Ephedrine (EPH) is a sympathomimetic drug that showed adverse effects on different body organs such as heart. Casuarinin (CAS) is a polyphenolic agent that exhibits various biological as well as pharmacological properties. The current research was performed to explore the mitigative attributes of CAS against EPH instigated sub-chronic cardiotoxicity. Thirty-six Sprague Dawley male rats were divided into control, EPH (20 mgkg-1), CAS (25 mgkg-1) + EPH (20 mgkg-1), and CAS (20 mgkg-1) alone administered group. Our findings revealed that EPH exposure provoked the gene expression of renin (REN), angiotensinogen (AGT), angiotensin I (Ang I), angiotensin II (Ang II), angiotensin II receptor type 1 (AGTR1), aldosterone synthase (CYP11B2), and mineralocorticoid receptor (NR3C2). The enzymatic activities of heme-oxygenase-1 (HO-1), glutathione peroxidase (GPx) (54.30 %), superoxide dismutase (SOD) (62.38 %), glutathione reductase (GSR) (54.80 %), catalase (CAT) (67.54 %), glutathione (GSH) (62.14 %) and glutathione S-transferase (GST) (44.25 %) were suppressed while the concentrations of reactive oxygen species (ROS) (2518.52 %) and malondialdehyde (MDA) (2654.55 %) were provoked after EPH intoxication. Besides, the EPH exposure exacerbated the concentration of N-terminal pro-B-type natriuretic peptide (ProBNP) (179.39), creatine kinase-myocardial band (CK-MB) (133.55 %), creatine phosphokinase (CPK) (180.72 %), C-reactive protein (CRP) (348.34 %), troponin-T (TnT) (1210.91 %), lactate dehydrogenase (LDH) (518.47 %), troponin-I (TnI) (1266.67 %) and brain natriuretic peptide (BNP) (243.34 %). The expression of Bax, and Caspase-3 were augmented while the expression of Bcl-2 was diminished after EPH administration. Moreover, EPH escalates the levels of interleukin-1beta (IL-1β) (471.71 %), cyclooxygenase-2 (COX-2) (304.16 %), tumor necrosis factor-alpha (TNF-α) (219.96 %), interleukin-6 (IL-6) (316.76 %), and nuclear factor-kappa B (NF-κB) (343.59 %) as well as significantly (p < 0.05) dysregulated the normal histology of cardiac tissues. Nevertheless, CAS treatment notably alleviated EPH instigated sub-chronic cardiac damage through the regulation of RAAS, oxidative stress, apoptosis, and inflammation. These findings suggest that CAS could be employed as cardioprotective agent against EPH intoxication.
期刊介绍：
Toxicon has an open access mirror Toxicon: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. An introductory offer Toxicon: X - full waiver of the Open Access fee.
Toxicon''s "aims and scope" are to publish:
-articles containing the results of original research on problems related to toxins derived from animals, plants and microorganisms
-papers on novel findings related to the chemical, pharmacological, toxicological, and immunological properties of natural toxins
-molecular biological studies of toxins and other genes from poisonous and venomous organisms that advance understanding of the role or function of toxins
-clinical observations on poisoning and envenoming where a new therapeutic principle has been proposed or a decidedly superior clinical result has been obtained.
-material on the use of toxins as tools in studying biological processes and material on subjects related to venom and antivenom problems.
-articles on the translational application of toxins, for example as drugs and insecticides
-epidemiological studies on envenoming or poisoning, so long as they highlight a previously unrecognised medical problem or provide insight into the prevention or medical treatment of envenoming or poisoning. Retrospective surveys of hospital records, especially those lacking species identification, will not be considered for publication. Properly designed prospective community-based surveys are strongly encouraged.
-articles describing well-known activities of venoms, such as antibacterial, anticancer, and analgesic activities of arachnid venoms, without any attempt to define the mechanism of action or purify the active component, will not be considered for publication in Toxicon.
-review articles on problems related to toxinology.
To encourage the exchange of ideas, sections of the journal may be devoted to Short Communications, Letters to the Editor and activities of the affiliated societies.
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