Effect of light-emitting diodes, platelet-rich plasma, and their combination on the activity of sheep tenocytes.

Healthy tendons play an important role in joint movements and subjected to a group of pathologies called tendinopathy due to multiple factors. Tendons have a slowly repairing process due to the low vascularity and cellularity. Treatment options aimed at potentiating the healing response and relieving symptoms. Phototherapy and platelet-rich plasma were novel treatment modalities in tendons based on photobiomodulation and growth factors during healing, and the results were encouraging suggesting calibrating treatment parameters. This study utilizes cell culture to explore the potential effect of light-emitting diode and/or growth factors in the form of platelet-rich plasma (PRP) on the activity of tenocytes isolated from sheep Achilles tendons by measuring the cell metabolism and cell mobility using cell viability and migration assays to proof safety and confirm activity. Results showed that sheep tenocyte-cultured groups treated with 5% platelet-rich plasma alone or combined with 4 J/cm2 light-emitting diode have increased viability significantly when compared to control group after a 48 h, while light-emitting diode treatment has not decreased cell migration significantly when compared with control. Result suggests that using platelet-rich plasma alone or combined with light-emitting diode might have potential to enhance healing response at the conditions applied. PRP could enhance proliferation while LED could enhance migration and proliferation. Further research is needed at longer durations.

Oxidative stress: a key contributor to diabetic cardiomyopathy.

Diabetes and its associated complications are major known health disorders. Diabetes mellitus increases the risk of cardiovascular morbidity and mortality by promoting cardiomyopathy. It appears to arise as a result of the diabetic state, at times independent of vascular or valvular pathology. It manifests initially as asymptomatic diastolic dysfunction, which progresses to symptomatic heart failure. The compliance of the heart wall is decreased and contractile function is impaired. The pathophysiology of diabetic cardiomyopathy is incompletely understood but appears to be multifactorial in origin. Several hypotheses have been proposed, including oxidative stress, inflammation, endothelial dysfunction, metabolic derangements, abnormalities in ion homeostasis, alterations in structural proteins, and interstitial fibrosis. Amongst these various mechanisms, an increase in reactive oxygen species, leading to oxidative stress, has received significant experimental support. This review focuses on the role of oxidative stress in the pathogenesis of diabetic cardiomyopathy and the potential of antioxidant therapy.

A concise description of cardioprotective strategies in doxorubicin-induced cardiotoxicity.

Doxorubicin (Dox) is frequently used as a frontline chemotherapeutic agent against a variety of cancers. Tremendous progress has been made on its optimal usage over the last 40 years. However, cardiotoxicity still remains a major concern. The great promise in this matter is that the mechanisms leading to antitumor activity appear to be different from those leading to Dox-induced cardiomyopathy. In this regard, various cardioprotective agents have been discussed. Attention should be drawn to probucol, a lipid-lowering agent with potent antioxidant properties, which provides complete protection against Dox-induced cardiomyopathy in rats without interfering with the antitumor properties of Dox in an experimental setting. Clinical trials employing Dox therapy in combination with probucol are needed to determine whether the outstanding findings in animal experiments can be extrapolated to clinical results. We have much further to go before the establishment of cancer therapies without any risk of cardiac side effects.