the-causal-effects-plasma-metabolites-on-achilles-tendon-injury

The Causal Effects of Plasma Metabolites on Achilles Tendon Injury: A Mendelian Randomization Study

To investigate the causal effects of plasma metabolites on the progression and recovery of Achilles tendon injury (ATI), Mendelian randomization (MR) was ...

Ningxia medical university

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. However, the function of 91 H in osteosarcoma remains unclear.

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

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. Flow cytometry and western blot assay were performed to detect the effect of DEX on the apoptosis of BMSCs. Quantitative real-time PCR and western blot assay were performed to detect the effect of DEX on the expression of endoplasmic reticulum stress (ERS)-related genes. Immunoblotting analysis was conducted for detecting the nuclear-cytoplasmic distribution of Nrf2. DEX could significantly inhibit the proliferation of BMSCs and promote apoptosis of BMSCs. DEX could increase the expression of PERK, ATF6, and IRE1a, and induce nuclear translocation of Nrf2. The addition of ML385 could reverse the effect of DEX on BMSCs. DEX could activate the PERK-Nrf2 pathway to promote ERS and finally affect the cell proliferation and apoptosis of BMSCs.

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

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

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

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. Diabetic mice were used to construct wound healing models. Recombinant TGF-β1 was used to promote wound healing in diabetic mice. FSL-1 was applied to activate NF-κB to verify the mechanism. High glucose inhibited cell viability and migration ability, promoted the expression of TNF-α, IL-6 and IL-1β, induced the activation of NF-κB pathway in fibroblasts. Inhibition of NF-κB not only blocked the decrease in cell viability and migration ability induced by high glucose, but also relieved the release of inflammatory factors. TGF-β1 activated the TGF-β1/Smad pathway and promoted wound healing in diabetic mice. Activating the NF-κB pathway not only inhibited the activation of the TGF-β1/Smad pathway, but also alleviated the promoting effect of TGF-β1 on wound healing. In a high glucose environment, the activation of NF-κB may inhibit the function of fibroblasts by inhibiting the TGF-β1/Smad pathway, resulting in poor wound healing.

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

This study investigated the impact of antibiotics on the therapeutic efficacy of PD-1 inhibitors and their association with the intestinal microbiota. Using a Hepa1-6 hepatocellular carcinoma mouse model, various antibiotics (vancomycin, colistin, and combination antibiotics) were administered alongside a PD-1 inhibitor. The results indicated that antibiotic treatment significantly altered the intestinal microbiota composition, with vancomycin and the combination antibiotics notably reducing PD-1 inhibitor efficacy. 16S rRNA sequencing revealed that antibiotic-induced selective pressure profoundly impacted both the diversity and abundance of the microbiota. Specifically, the relative abundance of Bacteroidetes and Firmicutes was significantly diminished following vancomycin treatment, correlating with reduced PD-1 inhibitor efficacy. Further analysis of the tumor immune microenvironment revealed no significant changes in the CD8 T cell ratio, TGF-β, IL-6, IL-17, or PD-1 levels. However, the proportion of CD4 T cells was markedly lower in the combination antibiotic group, and the expression of pro-inflammatory cytokines IFN-γ and IL-2 was substantially decreased across all antibiotic-treated groups. These findings suggest that alterations in specific intestinal bacterial populations, likely through modulation of pro-inflammatory cytokine levels in the tumor immune microenvironment, compromise immunotherapy effectiveness. This study highlights the critical role of healthy intestinal microbiota in optimizing tumor immunotherapy efficacy and emphasizes the need for careful consideration of antibiotic use in such treatments. Moreover, it provides novel insights into the mechanisms by which antibiotics may interfere with immunotherapy, laying the groundwork for optimizing anti-tumor immunotherapy strategies.

Article	Year
Knockdown of 91 H Suppresses the Tumorigenesis of Osteosarcoma via Inducing Methylation of CDK4 Promoter. Technology in cancer research & treatment\| PubMed ID: 33499776	2021
Dexamethasone promotes the endoplasmic reticulum stress response of bone marrow mesenchymal stem cells by activating the PERK-Nrf2 signaling pathway. Pharmacology research & perspectives\| PubMed ID: 34038621	2021
Comparison of the Effects of Open Surgery and Minimally Invasive Surgery on the Achilles Tendon Rupture Healing Based on Angiogenesis. Computational intelligence and neuroscience\| PubMed ID: 36093506	2022
Inhibition of TGFβ1/Smad pathway by NF-κB induces inflammation leading to poor wound healing in high glucose. Cells & development\| PubMed ID: 36307062	2022
Study on the Effect of Antibiotics on the Efficacy of PD-1 Inhibitors and Its Regulatory Mechanism via the Intestinal Bacterial Community. Biochemical genetics\| PubMed ID: 40646292	2025

Fan Gong

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