Expression of Concern: Preventive effect of nerolidol on isoproterenol induced myocardial damage in Wistar rats: Evidences from biochemical and histopathological studies

Abstract

The present study aimed at investigating the protective effects of nerolidol (NRD) against myocardial infarction (MI) induced by isoproterenol (ISO) in Wistar rats. The rats were randomly divided into five groups, each group consisting of six rats. Group I were treated as control rats, group II received NRD (200 mg/kg b.w.) by intragastric intubation for 21 days, group III received ISO (60 mg/kg b.w) subcutaneously (s.c) for two consecutive days on 22nd and 23rd day, group IV and V received NRD (100 and 200 mg/kg b.w) as in group II and additionally ISO was given for two consecutive days (22nd and 23rd). On 24th day all the rats were sacrificed by cervical dislocation and the blood and heart samples were collected. In the present study, ISO‐induced myocardial damage was indicated by the changes in body weight, heart weight and the cardiac and hepatic marker enzymes such as creatine kinase (CK), creatine kinase‐MB (CK‐MB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and troponin T and I (cTnT, cTnI) in the serum. In addition, the levels of lipid peroxidation products such as thiobarbituric acid reactive substances (TBARS), conjugated dines (CD), and lipid hydroperoxides (LHPs) increased significantly in the plasma and heart tissue. Activities of enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione‐S‐transferase (GST) in erythrocytes and heart tissue and the levels of nonenzymatic antioxidants like vitamin C, vitamin E, and reduced glutathione (GSH) in plasma and heart tissue were decreased in ISO‐induced rats. Histopathological observations were also supported with the biochemical parameters. Pretreatment with NRD at different doses (100 and 200 mg/kg b.w) for 21 days prevented the above changes induced by ISO. The 200 mg/kg b.w of NRD was more pronounced than the other dose and brought back all the above parameters near to normalcy.

Arbutin prevents alterations in mitochondrial and lysosomal enzymes in isoproterenol-induced myocardial infarction: An in vivo study

“…Elevated levels of blood cholesterol and its buildup in cardiac tissue are well connected with cardiovascular damage. 49 In the present study, ISOadministered rats showed a significant increase in the levels of TC, TG, and FFA in myocardium and plasma while the levels of PLs increased in the plasma and decreased in heart, which is in line with the previous studies. 15 ISO has been reported to produce stress in the myocardium due to the production of free radicals by its auto-oxidation, which leads to membrane degradation.…”

Untitled

“…In our study, we noticed the elevated levels of cTnT and cTnI and the increased activities of the AST, ALT, CK, CK-MB, and LDH in serum of ISO-induced rats; it might be due to the cardiac damage induced by ISO. Our results are consistent with a previous report by Vennila et al, (2010) 31 . ARB pretreatment prevented theses increase in ISO administered rats.…”

Nerolidol Attenuates Oxidative Stress, Inflammation, and Apoptosis by Modulating Nrf2/MAPK Signaling Pathways in Doxorubicin-Induced Acute Cardiotoxicity in Rats

“…It has been shown to activate antioxidant signaling pathways and attenuate inflammatory and apoptotic signaling pathways, as well as exert cytoprotective properties by improving antioxidant defense [ 29 ] and exerting anti-inflammatory effects [ 23 , 30 , 31 ]. Recently, NERO has been shown to attenuate oxidative stress, inflammation, fibrosis, and apoptosis in cardiotoxicity induced by cyclophosphamide, a chemotherapeutic agent [ 32 ], isoproterenol-induced myocardial infarction [ 33 ], and modulate contractile function of the atrium [ 34 ]. Additionally, NERO has been shown effective as an anticancer agent due to its potential to modulate important molecular targets of cell survival and proliferation [ 35 ], as well as act as a chemosensitizer in cancer cells [ 36 , 37 , 38 ].…”