Drug-loaded hyaluronic acid hydrogel as a sustained-release regimen with dual effects in early intervention of tendinopathy.

Resulting from accumulative microtrauma, impaired healing and oxidative stress, tendinopathy is a debilitating and relentlessly deteriorating disease that greatly affects daily function and quality of life. Current therapy usually provides symptomatic relief only. Sufferers undergo repetitive and protracted treatment courses that rarely alter the disease process. We aim to develop a sustained-release regimen with an intrinsic therapeutic effect in tendinopathy treatment, using oxidised hyaluronic acid/adipic acid dihydrazide hydrogel (HA hydrogel) as both the drug carrier and a mitigating agent of symptoms. We show that HA hydrogel can mitigate tendinopathy changes both in vitro (mechanically induced tendinopathy model) and in vivo (collagenase-induced tendinopathy model). A potent anti-oxidative (pigallocatechin gallate) incorporated into HA hydrogel conferred an additional protective effect in both models. The results indicate that when administered early, combined medications targeting different pathogenesis pathways can resolve tendinopathy. Although facilitating the healing process and mitigating oxidative stress are promising therapeutic strategies, the most effective regimen for tendinopathy treatment has to be determined yet. The established experimental model and drug carrier system provide a platform for exploring new therapeutics against this debilitating disease.

Canine heat shock protein 27 promotes proliferation, migration, and doxorubicin resistance in the canine cell line DTK-F.

Canine mammary tumors (CMTs) are the most common type of tumors in female dogs. Heat shock proteins are highly expressed in many cancers and are involved in tumor progression and chemoresistance in CMTs; however, the biological role of canine heat shock protein 27 (cHSP27) in CMTs has not been thoroughly characterized. This study investigated the roles of cHSP27 in cell growth, migration, anchorage, and resistance to doxorubicin (DOX) using DTK-F cells, a CMT cell line that does not express cHSP27. DTK-F cells were transfected with cHSP27 and stable overexpression was established. A mouse monoclonal antibody against cHSP27 was also produced. The biological functions of cHSP27 in DTK-F cells were then evaluated using a variety of assays. Overexpression of cHSP27 was associated with increased cell proliferation, clone formation, migration, and decreased DOX sensitivity. In conclusion, these data provide evidence that cHSP27 overexpression can promote anchorage-independent growth, migration, and increased DOX resistance in CMT cells.