Inhibition of TGFβ1/Smad pathway by NF-κB induces inflammation leading to poor wound healing in high glucose.

This study mainly analyzed the relationship between nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and transforming growth factor-β (TGFβ1)/Smad under high glucose environment and its influence on wound healing. Fibroblast NIH-3T3 was used to analyze the effect of high concentration glucose (20 nmol/mL) on cell viability, migration ability, inflammation level and NF-κB pathway. Pyrrolidinedithiocarbamate (PDTC) was used to inhibit NF-κB for rescue experiments.

Comparison of the Effects of Open Surgery and Minimally Invasive Surgery on the Achilles Tendon Rupture Healing Based on Angiogenesis.

Objective: To compare the effect of three different surgical methods on rabbit Achilles tendon rupture.

Methods: The Achilles tendon transection model was constructed by cutting off the inner half of the Achilles tendon. Rabbits were divided into 4 groups: model group, open surgery (OS) group, minimally invasive surgery (MS) group, and conservative treatment (CT) group.

MiR-192-5p Alleviated Fibrosis and Inflammatory Responses of Tendon Cells by Targeting NFAT5.

Objective: To explore the effect of microRNA (miR)-192-5p on the inflammatory and fibrotic responses of tendon cells.

Methods: Tendon cells were treated with transforming growth factor-1 (TGF-1). The expression of miR-192-5p and nuclear factor of activated T cells 5 (NFAT5) in tendon cells were detected by RT-qPCR.

Dexamethasone promotes the endoplasmic reticulum stress response of bone marrow mesenchymal stem cells by activating the PERK-Nrf2 signaling pathway.

The pathogenesis of steroid-induced avascular necrosis of femoral head (SANFH) is complex, and there is a lack of effective early prevention method. The aim of the present study was to evaluate the effect of dexamethasone (DEX) on the biological behavior of bone marrow mesenchymal stem cells (BMSCs) and to explore the possibility of DEX in the clinical treatment of SANFH. The effect of DEX on the proliferation of BMSCs was evaluated by Counting Kit-8 assay, western blot assay, and enzyme-linked immunosorbent assay.

Knockdown of 91 H Suppresses the Tumorigenesis of Osteosarcoma via Inducing Methylation of CDK4 Promoter.

Background: Osteosarcoma is the most leading primary malignancy of the bone in adolescents all over the world. Long non-coding RNA (lncRNA) 91 H has been reported to participated in multiple cancers. Meanwhile, lncRNA 91 H has been proved to be upregulated in osteosarcoma.