PMID- 30166919 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20201001 IS - 1319-0164 (Print) IS - 2213-7475 (Electronic) IS - 1319-0164 (Linking) VI - 26 IP - 2 DP - 2018 Feb TI - Roles of some antioxidants in modulation of cardiac myopathy induced by sodium nitrite via down-regulation of mRNA expression of NF-kappaB, Bax, and flt-1 and suppressing DNA damage. PG - 217-223 LID - 10.1016/j.jsps.2017.12.008 [doi] AB - The underlying pathology of cardiac damage involves various molecular and signaling pathways. Therefore, this study aimed to explore the role of Quercetin (Querc), alone or in combination with Melatonin (Melat) against cardiac damage induced by sodium nitrite (Sod nit), as well as to elucidate different signaling pathways. Querc and Melat were injected intraperitoneally (i.p.), followed by induction of hypoxia in rats by using a single dose of Sod nit (60 mg/kg, s.c.). Treatment with Sod nit significantly decreased hemoglobin (Hb) levels in blood. Pretreatment of hypoxic rats with Querc and/or Melat elevated the declined Hb concentration. The forementioned antioxidants also successfully ameliorated the alteration of heat shock protein 70 (HSP-70) and markers of cardiac injury, including troponin T (Trop. T), creatine kinase-MB (CK-MB), tumor necrosis factor-alpha (TNF alpha), and C-reactive protein (CRP) in the rats serum. Furthermore, RT-PCR revealed that these antioxidants successfully modulated mRNA expression of NF-kappaB, Bax, Bcl-2, and flt-1. They also regulated vascular endothelial growth factor (VEGF), the apoptosis marker caspase 3, and oxidative DNA damage in cardiac tissue, compared to Sod nit-intoxicated rats. The present biochemical results are reinforced by histopathological examination. IN CONCLUSION: The results reflected that treatment with Querc in combination with Melat was most effective in improving Sod nit-toxicity induced cardiac damage, thus confirming the promising role of this combination as an effective treatment for cardiac damage induced by other cardio-toxic agents. FAU - Fadda, Laila Mohamed AU - Fadda LM AD - Pharmacology Department, Faculty of Pharmacy, King Saud University, Riyadh, Saudi Arabia. FAU - Attia, Hala A AU - Attia HA AD - Pharmacology Department, Faculty of Pharmacy, King Saud University, Riyadh, Saudi Arabia. AD - Department of Biochemistry, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt. FAU - Al-Rasheed, Nouf Mohamed AU - Al-Rasheed NM AD - Pharmacology Department, Faculty of Pharmacy, King Saud University, Riyadh, Saudi Arabia. FAU - Ali, Hanaa Mahmoud AU - Ali HM AD - Department of Genetics and Cytology, National Research Center, Dokki, Egypt. AD - Common First Year Deanship, King Saud University, Riyadh, Saudi Arabia. FAU - Al-Rasheed, Nawal Mohamed AU - Al-Rasheed NM AD - Pharmacology Department, Faculty of Pharmacy, King Saud University, Riyadh, Saudi Arabia. AD - Department of Pharmaceutical Sciences, College of Pharmacy, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia. LA - eng PT - Journal Article DEP - 20171211 PL - Saudi Arabia TA - Saudi Pharm J JT - Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society JID - 9705695 PMC - PMC6111199 OTO - NOTNLM OT - Cardiac tissue OT - Comet assay OT - Hypoxia OT - Melatonin, Quercetin EDAT- 2018/09/01 06:00 MHDA- 2018/09/01 06:01 PMCR- 2017/12/11 CRDT- 2018/09/01 06:00 PHST- 2017/11/18 00:00 [received] PHST- 2017/12/10 00:00 [accepted] PHST- 2018/09/01 06:00 [entrez] PHST- 2018/09/01 06:00 [pubmed] PHST- 2018/09/01 06:01 [medline] PHST- 2017/12/11 00:00 [pmc-release] AID - S1319-0164(17)30216-5 [pii] AID - 10.1016/j.jsps.2017.12.008 [doi] PST - ppublish SO - Saudi Pharm J. 2018 Feb;26(2):217-223. doi: 10.1016/j.jsps.2017.12.008. Epub 2017 Dec 11.