Fig 1: Effects of PTE on cell protection in H9c2 cells. (A–L) Effects of PTE in anticancer drug (IC20)-treated H9c2 cells on cell viability (A), mtROS (B), mt4HNE (C), mtGPX4 (D), GSH/GSSG ratio (E), TFAM (F), mtHO1 (G), BVD production (H), mtFe (I), basal OCR (J), ATP (K), myogenin and SDS-MYL1 (L), mRNA expression of HO1 and FCH (M), and its semi-quantification. Error bar, standard deviation from three independent trials. Statistical difference was calculated by AVOVA. PTE, pterostilbene; SUN, sunitinib; LAP, lapatinib; 5FU, 5-fluorouracil; CDDP, cisplatin; C, control; mtROS, mitochondrial hydroxy radical; mt4HNE, mitochondrial 4-hydroxynonenal; mtGPX4, mitochondrial glutathione peroxidase-4; GSH, glutathione; GSSG, glutathione disulfide; TFAM, mitochondrial transcription factor A; HO1, haem oxygenase-1; FCH, ferrochelatase; BVD, biliverdin; mtFe, mitochondrial iron (II); OCR, oxygen consumption rate; SDS-MYL1, sodium dodecyl sulfate-soluble myosin light chain-1.
Fig 2: Effects of PTE on anticancer-drug-induced myocardial damages in rats. (A) Experimental protocol. F344 rats (5 weeks old, male) were treated with SUN (40 mg/kg BW, i.p.), LAP (40 mg/kg BW, i.p.), 5FU (30 mg/kg BW, i.p.), and CDDP (3 mg/kg BW, i.p.), with or without PTE (20 mg/kg BW, i.p.), twice a week for 4 weeks. (B) Heart weight, (C) SDS-MYL1, (D) mt4HNE, (E) mtGPX4, (F) GSH/GSSG ratio, (G) mtHO1, (H) mitochondrial total iron, (I) serum troponin T, and (J) time course of serum troponin T in 5FU-treated rats. (K) ATP. Error bar, standard deviation from 9 rats. Statistical difference was calculated by AVOVA. PTE: pterostilbene; SUN: sunitinib; LAP: lapatinib; 5FU: 5-fluorouracil; CDDP: cisplatin; C: control; BW: body weight; SDS-MYL1: sodium dodecyl sulfate-soluble myosin light chain-1; mt4HNE: mitochondrial 4-hydroxynonenal; mtGPX4: mitochondrial glutathione peroxidase-4; GSH: glutathione; GSSG: glutathione disulfide; mtHO1: mitochondrial haem oxygenase-1; BVD: biliverdin; OCR: oxygen consumption.
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