000 a
999 _c16221
_d16221
003 OSt
005 20220204115324.0
008 220204b xxu||||| |||| 00| 0 eng d
040 _aAIKTC-KRRC
_cAIKTC-KRRC
100 _915857
_aEmeka, Promise Madu
245 _aAttenuation of cardiomyopathy induced in sub-chronic exposure of acrolein by sulforaphane via indirect ppary expression promoter
250 _aVol.55(4), Oct-Dec
260 _aKarnataka
_bAssociation of Pharmaceutical Teachers of India (APTI)
_c2021
300 _a1048-1059p.
520 _aSulforaphane (SPN) is reported to activate the Nrf2/Keap1 complex responsible for protein and gene expression promotion of various antioxidant enzymes. The present study examined the role of Nrf2 in modulating other signaling pathways involved in SPN’s attenuation of acrolein (ACL)-induced cardiomyopathy in rats. Forty-two rat was categorized into seven 4-week treatment groups: control, SPN, losartan (LTN), ACL, ACL+SPN, ACL+LTN, and ACL+SPN+LTN. Heart samples were harvested for analysis; cardiac oxidative and injury biomarker levels and histopathological examination were undertaken. PPARγ, Nrf2, NF-κB, COX-2, and CYP2E1 protein expressions were examined. Results show that SPN and SPN+LTN reduced GSH, catalase, and lipid peroxidation compared to the ACL-treated group. Also, levels of creatine kinase-MB, cardiac troponin, and caspase 3 induced by ACL were all attenuated. Altered cardiac tissue pathophysiology by ACL was alleviated. SPN+LTN significantly increased Nrf2 expression via PPARγ action but decreased NF-κB and COX-2 expressions. Also, ACLincreased CYP2E1 expression was significantly attenuated by the SPN+LTN combination. For the first time, it suggests that SPN+LTN might offer a better therapeutic alternative to ACL-induced cardiomyopathy by activating Nrf2 via PPARγ and reducing NF-κB/COX- 2/CYP2E1 expressions.
650 0 _94639
_aPHARMACEUTICS
700 _915858
_aHairul-Islam Mohamed Ibrahim
773 0 _dBengluru Association of Pharmaceutical Teachers of India (APTI)
_tIndian journal of pharmaceutical education and research
_x0019-5464
856 _uhttps://www.ijper.org/sites/default/files/IndJPhaEdRes-55-4-1048.pdf
_yClick here
942 _2ddc
_cAR