ABSTRACT
Dental implants have been extensively used in patients with defects or loss of dentition. However, the loss or failure of dental implants is still a critical problem in clinic. Therefore, many methods have been designed to enhance the osseointegration between the implants and native bone. Herein, the challenge and healing process of dental implant operation will be briefly introduced. Then, various surface modification methods and emerging biomaterials used to tune the properties of dental implants will be summarized comprehensively.
ABSTRACT
Atorvastatin is the most prescribed cholesterol-lowering statin, while caffeine enhances chemo-sensitivity and induces apoptosis of tumor cells through its DNA repair-inhibiting effect. The present study investigated the effects and mechanisms of atorvastatin and caffeine in combination on human prostate cancer cells cultured in vitro. Cell growth were determined by the trypan blue exclusion assay. The cell apoptosis and colony formation were determined by morphological assessment. The ability of cell migration and invasion were performed using a scratch wound-healing and Transwell assay. Tumorspheres were formed in suspension under the condition of non-adherence and serum-free medium. Finally, the western blot assay was used to determine the levels of proteins. The combination synergistically suppressed proliferation and induced apoptotic death. Meanwhile, the migration, invasion, and the formation of tumorspheres were significantly inhibited by the combination. We found that atorvastatin and caffeine in combination downregulated phospho-Akt, phospho-Erk1/2, anti-apoptotic Bcl-2 and Survivin protein levels. Results of the present study indicate treatment with the combination of caffeine and atorvastatin may be an effective strategy for inhibiting the growth of prostate cancer and should be evaluated clinically.
Subject(s)
Apoptosis/drug effects , Atorvastatin/pharmacology , Caffeine/pharmacology , Cell Movement/drug effects , Prostatic Neoplasms/pathology , Cell Proliferation/drug effects , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Male , PC-3 Cells , Phosphodiesterase Inhibitors/pharmacologyABSTRACT
Chronic periodontitis is associated with Porphyromonas gingivalis (P. gingivalis) infection. Hyaluronic Acid (HA), a critical component of the extracellular matrix, exhibits anti-inflammatory and wound-healing properties. This study aimed to investigate the effect of various molecular weights of HA (30, 300 and 1300 kDa) on P. gingivalis-induced inflammatory and wound-healing responses in human gingival fibroblasts (HGFs). Cell cytotoxicity and proliferation were assessed by Lactate dehydrogenase and MTT assays, respectively. An enzyme linked immunosorbent assay was used to detect the levels of interleukin (IL) -1ß, IL-6, IL-8, IL-4 and IL-10. Cell migration was evaluated with a scratch wound healing assay. The expression of nuclear factor kappa B (NF-кB), IкBα, p38 and extracellular signal-regulated kinase (ERK) were analyzed with Western blotting. The results showed that P. gingivalis (1.6 × 106 CFU/mL) and HA (1, 2, 5 and 10 mg/mL) exhibited no toxicity to the HGFs. The 1300 kDa HA inhibited P. gingivalis-induced IL-1ß, IL-6, IL-8, IL-4 and IL-10 production in a dose-dependent manner, while the 30 and 300 kDa HA did not have an effect. Meanwhile, cell migration was significantly promoted by the 30 and 1300 kDa HA. Furthermore, the 1300 kDa HA inhibited NF-κB expression, IκBα degradation and P. gingivalis-induced ERK and P38 activation. Therefore, our study suggests that high molecular weight HA may have beneficial effects on periodontal inflammation and oral wounds.
Subject(s)
Cell Movement/drug effects , Fibroblasts/drug effects , Gingiva/drug effects , Hyaluronic Acid/pharmacology , Inflammation/drug therapy , MAP Kinase Signaling System/drug effects , Molecular Weight , Porphyromonas gingivalis/pathogenicity , Anti-Inflammatory Agents/pharmacology , Cell Line , Cell Proliferation/drug effects , Cell Survival/drug effects , Gingiva/cytology , Humans , Hyaluronic Acid/administration & dosage , Hyaluronic Acid/chemistry , Interleukin-10/metabolism , Interleukin-1beta/metabolism , Interleukin-4/metabolism , Interleukin-6/metabolism , Interleukin-8/metabolism , NF-kappa B/metabolism , Periodontal Diseases/drug therapy , Wound Healing/drug effectsABSTRACT
We investigated the functional role and mechanism of miR-1-3p and DKK1 in oral squamous cell carcinoma (OSCC) cells. The level of miR-1-3p and DKK1 expression were detected in OSCC tissues and cells using reverse-transcription - quantitative PCR and Western blot. A dual luciferase reporter gene assay was applied to confirm the targeting relationship between miR-1-3p and DKK1. Functional assays, including MTT, Transwell, colony formation, and flow cytometry analysis were conducted to verify their effect on cell progressions. MTT, colony formation, and Transwell assays indicated that the proliferation, migration, and invasion of SCC-4 cells was impaired with high miR-1-3p expression but promoted with high DKK1 expression. The results from cell cycle analysis and annexin-V-PI assays for apoptosis suggested that miR-1-3p suppressed the transit of SCC-4 cells from G0/G1 to S and induced apoptosis. In summary, miR-1-3p suppressed the progression of OSCC by inhibiting DKK1 expression.
Subject(s)
Carcinoma, Squamous Cell/genetics , Cell Movement , Cell Proliferation/genetics , Intercellular Signaling Peptides and Proteins/genetics , MicroRNAs/genetics , Mouth Neoplasms/genetics , Apoptosis/genetics , Cell Cycle/genetics , Cell Line, Tumor , Cell Movement/genetics , Gene Expression Regulation, Neoplastic/genetics , Humans , Mouth Neoplasms/pathologyABSTRACT
Metformin is a commonly used drug for the treatment of type II diabetes and atorvastatin is the most prescribed cholesterol-lowering statin. The present study investigated the effects and mechanisms of metformin and atorvastatin in combination on human prostate cancer cells cultured in vitro and grown as xenograft tumor in vivo. Metformin in combination with atorvastatin had stronger effects on growth inhibition and apoptosis in PC-3 cells than either drug alone. The combination also potently inhibited cell migration and the formation of tumorspheres. Metformin and atorvastatin in combination had a potent inhibitory effect on nuclear factor-kappaB (NF-κB) activity and caused strong decreases in the expression of its downstream anti-apoptotic gene Survivin. Moreover, strong decreases in the levels of phospho-Akt and phosphor-extracellular signal-regulated kinase (Erk)1/2 were found in the cells treated with the combination. The in vivo study showed that treatment of severe combined immunodeficient (SCID) mice with metformin or atorvastatin alone resulted in moderate inhibition of tumor growth while the combination strongly inhibited the growth of the tumors. Results of the present study indicate the combination of metformin and atorvastatin may be an effective strategy for inhibiting the growth of prostate cancer and should be evaluated clinically.
