Recombinant Troponin I-Cardiac [His]

The present study aimed to investigate whether arginine (Arg) promotes porcine type I muscle fibres formation via improving mitochondrial biogenesis. In the in vivo study, a total of sixty Duroc x Landrace x Yorkshire weaning piglets with an average body weight of 6 center dot 55 (sd 0 center dot 36) kg were randomly divided into four treatments and fed with a basal diet or a basal diet supplemented with 0 center dot 5, 1 center dot 0 and 1 center dot 5 % l-Arg, respectively, in a 4-week trial. Results showed that dietary supplementation of 1 center dot 0 % Arg significantly enhanced the activity of succinate dehydrogenase, up-regulated the protein expression of myosin heavy chain I (MyHC I) and increased the mRNA levels of MyHC I, troponin I1, C1 and T1 (Tnni1, Tnnc1 and Tnnt1) in longissimus dorsi muscle compared with the control group. In addition, ATPase staining analysis indicated that 1 center dot 0 % Arg supplementation significantly increased the number of type I muscle fibres and significantly decreased the number of type II muscle fibres. Furthermore, 1 center dot 0 % Arg supplementation significantly up-regulated PPAR-gamma coactivator-1 alpha (PGC-1 alpha), sirtuin 1 and cytochrome c (Cytc) protein expressions, increased PGC-1 alpha, nuclear respiratory factor 1 (NRF1), mitochondria transcription factor B1 (TFB1M), Cytc and ATP synthase subunit C1 (ATP5G) mRNA levels and increased mitochondrial DNA content. In the in vitro study, mitochondrial complex I inhibitor rotenone (Rot) was used. We found that Rot annulled Arg-induced type I muscle fibres formation. Together, our results provide for the first time the evidence that Arg promotes porcine type I muscle fibres formation through improvement of mitochondrial biogenesis.

Shenmai formula (SM) has been a traditional medicinal remedy for treating cardiovascular diseases in China for 800 years; however, its mechanism of action remains unclear. To explore the mechanism underlying cardioprotective effects of SM, iTRAQ:based proteomic approach was applied to analyze protein of myocardium in rats with myocardial ischemic injury. Upon treatment with SM and its two major components Red ginseng (RG) and Radix Ophiopogonis (OP), 101 differentially expressed proteins were filtered from a total of 712 detected and annotated proteins. They can be classified according to their locations and functions, while most of them are located in intracellular organelle, participating in cellular metabolic process. The functions of them are mostly associated with mitochondrial oxidative phosphorylation/respiration. The differentially expressed proteins were validated by liquid chromatography tandem mass spectrometry and Western blotting (ATP5D, NDUFB10, TNNC1). Further in vitro experiments found that SM could attenuate hypoxia induced impairment of mitochondrial membrane potential and cellular ATP concentration in neonatal rat ventricular myocytes. Interestingly, the result of quantitative mitochondrial biogenesis assays revealed that SM had dominant positive effects on the maximum respiration, ATP-coupled respiration, and spare capacity of mitochondria in response to hypoxia. Hence, our findings suggest that SM promotes mitochondrial function to protect cardiomyocytes against hypoxia, which provides a possible illustration for conventional botanical therapy on a molecular level.