Peri-implantitis is an inflammatory disease similar to periodontitis, caused by biofilms formed on the surface of dental implants. This inflammation can spread to bone tissues and result in bone ...loss. Therefore, it is essential to inhibit the formation of biofilms on the surface of dental implants. Thus, this study examined the inhibition of biofilm formation by treating TiO2 nanotubes with heat and plasma. Commercially pure titanium specimens were anodized to form TiO2 nanotubes. Heat treatment was performed at 400 and 600 °C, and atmospheric pressure plasma was applied using a plasma generator (PGS-200, Expantech, Suwon, Republic of Korea). Contact angles, surface roughness, surface structure, crystal structure, and chemical compositions were measured to analyze the surface properties of the specimens. The inhibition of biofilm formation was assessed using two methods. The results of this study showed that the heat treatment of TiO2 nanotubes at 400 °C inhibited the adhesion of Streptococcus mutans (S. mutans), associated with initial biofilm formation, and that heat treatment of TiO2 nanotubes at 600 °C inhibited the adhesion of Porphyromonas gingivalis (P. gingivalis), which causes peri-implantitis. Applying plasma to the TiO2 nanotubes heat-treated at 600 °C inhibited the adhesion of S. mutans and P. gingivalis.
The alternative antibacterial treatment photothermal therapy (PTT) significantly affects oral microbiota inactivation. In this work, graphene with photothermal properties was coated on a zirconia ...surface using atmospheric pressure plasma, and then the antibacterial properties against oral bacteria were evaluated. For the graphene oxide coating on the zirconia specimens, an atmospheric pressure plasma generator (PGS-300, Expantech, Suwon, Republic of Korea) was used, and an Ar/CH
gas mixture was coated on a zirconia specimen at a power of 240 W and a rate of 10 L/min. In the physiological property test, the surface properties were evaluated by measuring the surface shape of the zirconia specimen coated with graphene oxide, as well as the chemical composition and contact angle of the surface. In the biological experiment, the degree of adhesion of
(
) and
(
) was determined by crystal violet assay and live/dead staining. All statistical analyzes were performed using SPSS 21.0 (SPSS Inc., Chicago, IL, USA). The group in which the zirconia specimen coated with graphene oxide was irradiated with near-infrared rays demonstrated a significant reduction in the adhesion of
and
compared with the group not irradiated. The oral microbiota inactivation was reduced by the photothermal effect on the zirconia coated with graphene oxide, exhibiting photothermal properties.
Veratrum maackii (VM), a perennial plant in the Melanthiaceae family, has anti-hypertensive, anti-cholinergic, anti-asthmatic, anti-tussive, anti-fungal, anti-melanogenesis, and anti-tumor ...activities. Here, we investigated the therapeutic effect of VM on benign prostatic hyperplasia (BPH) in human normal prostate cell line (WPMY-1) and a testosterone propionate-induced BPH animal model. WPMY-1 cells were treated with VM (1–10 µg/mL) and testosterone propionate (100 nM). BPH in rats was generated via daily subcutaneous injections of testosterone propionate (3 mg/kg) dissolved in corn oil, for 4 weeks. VM (150 mg/kg) was administered daily for 4 weeks by oral gavage concurrently with the testosterone propionate. All rats were sacrificed and the prostates were dissected, weighed, and subjected to histological, immunohistochemical, and biochemical examinations. Immunoblotting experiments indicated that WPMY-1 cells treated testosterone propionate had increased expression of prostate specific antigen (PSA) and androgen receptor (AR), and treatment with VM or finasteride blocked this effect. In rat model, VM significantly reduced prostate weight, prostatic hyperplasia, prostatic levels of dihydrotestosterone (DHT), and expression of proliferation markers such as proliferating cell nuclear antigen (PCNA) and cyclin D1, but increased the expression of pro-apoptotic Bcl-2-associated X protein (Bax) and the cleavage of caspase-3. VM administration also suppressed the testosterone propionate-induced activation of nuclear factor-kappaB (NF-κB). Our results indicate that VM effectively represses the development of testosterone propionate-induced BPH, suggesting it may be a useful treatment agent for BPH.
Impaired macroautophagy/autophagy has been implicated in experimental and human nonalcoholic steatohepatitis (NASH). However, the mechanism underlying autophagy dysregulation in NASH is largely ...unknown. Here, we investigated the role and mechanism of TXNIP/VDUP1 (thioredoxin interacting protein), a key mediator of cellular stress responses, in the pathogenesis of NASH. Hepatic TXNIP expression was upregulated in nonalcoholic fatty liver disease (NAFLD) patients and in methionine choline-deficient (MCD) diet-fed mice, as well as in palmitic acid (PA)-treated hepatocytes. Upregulation of hepatic TXNIP was positively correlated with impaired autophagy, as evidenced by a decreased number of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3 beta) puncta and increased SQSTM1/p62 (sequestosome 1) expression. Deletion of the Txnip gene enhanced hepatic steatosis, inflammation, and fibrosis, accompanied by impaired autophagy and fatty acid oxidation (FAO) in MCD diet-fed mice. Mechanistically, TXNIP directly interacted with and positively regulated p-PRKAA, leading to inactivation of MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1) and nuclear translocation of TFEB (transcription factor EB), which in turn promoted autophagy. Inhibition of MTORC1 by rapamycin induced autophagy and increased the expression levels of FAO-related genes and concomitantly attenuated lipid accumulation in PA-treated txnip-knockout (KO) hepatocytes, which was further abolished by silencing of Atg7. Rapamycin treatment also attenuated MCD diet-induced steatosis, inflammation, and fibrosis with increased TFEB nuclear translocation and restored FAO in txnip-KO mice. Our findings suggest that elevated TXNIP ameliorates steatohepatitis by interacting with PRKAA and thereby inducing autophagy and FAO. Targeting TXNIP may be a potential therapeutic approach for NASH.
Abbreviations: ACOX1: acyl-Coenzyme A oxidase 1, palmitoyl; ACSL1: acyl-CoA synthetase long-chain family member 1; ACTA2/α-SMA: actin, alpha 2, smooth muscle, aorta; ACTB: actin beta; ADGRE1/F4/80: adhesion G protein-coupled receptor E1; AMPK: AMP-activated protein kinase; ATG: autophagy-related; BafA1: bafilomycin A1; COL1A1/Col1α1: collagen, type I, alpha 1; CPT1A: carnitine palmitoyltransferase 1a, liver; CQ: chloroquine; DGAT1: diacylglycerol O-acyltransferase 1; DGAT2: diacylglycerol O-acyltransferase 2; ECI2/Peci: enoyl-Coenzyme A isomerase 2; EHHADH: enoyl-Coenzyme A, hydratase/3-hydroxyacyl Coenzyme A dehydrogenase; FAO: fatty acid oxidation; FASN: fatty acid synthase; FFA: free fatty acids; GFP: green fluorescent protein; GK/GYK: glycerol kinase; GOT1/AST: glutamic-oxaloacetic transaminase 1, soluble; GPAM: glycerol-3-phosphate acyltransferase, mitochondrial; GPT/ALT: glutamic pyruvic transaminase, soluble; H&E: hematoxylin and eosin; IL1B/IL-1β: interleukin 1 beta; IL6: interleukin 6; IOD: integral optical density; KO: knockout; Leu: leupeptin; LPIN1: lipin 1; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MCD: methionine choline-deficient; MMP9: matrix metallopeptidase 9; mRNA: messenger RNA; MTORC1: mechanistic target of rapamycin kinase complex 1; NAFLD: nonalcoholic fatty liver diseases; NASH: nonalcoholic steatohepatitis; PA: palmitic acid; PPARA/PPARα: peroxisome proliferator activated receptor alpha; PPARG/PPARγ: peroxisome proliferator activated receptor gamma; qRT-PCR: quantitative real-time PCR; RPS6KB1/p70S6K1: ribosomal protein S6 kinase, polypeptide 1; RPTOR: regulatory associated protein of MTOR complex 1; SCD1: stearoyl-Coenzyme A desaturase 1; SEM: standard error of the mean; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TFEB: transcription factor EB; TG: triglyceride; TGFB/TGF-β: transforming growth factor, beta; TIMP1: tissue inhibitor of metalloproteinase 1; TNF/TNF-α: tumor necrosis factor; TXNIP/VDUP1: thioredoxin interacting protein; WT: wild-type
Improved dispersibility of zirconia nanoparticles (ZrO2 NPs) is crucial in many optical applications, but traditional dispersion methods using dispersants or devices can be problematic. In this ...study, we propose a simple and novel dispersion method that controls the crystalline phase through yttrium (Y3+) doping to improve dispersibility. The ZrO2 NPs colloidal sol was developed using three precursors – acetate-based zirconia (A-ZrO2), acetate-based 3-yttria stabilized zirconia (A-3YSZ), and chloride-based 3-yttria stabilized zirconia (C-3YSZ). The A-3YSZ exhibited the most superior dispersibility among the samples due to its low surface energy. Furthermore, it maintained dispersibility even though precursor concentration increased up to 6 wt%. Our results show that A-3YSZ is an effective inorganic filler for improving the refractive index of an acrylate-based coating solution. This is due to its excellent dispersibility and simple synthesis without requiring additional chemical modification and complicated dispersion processes.
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•Dispersibility control via the crystalline phase of YSZ.•Dispersibility was related to surface energy according to the crystalline phase.•Simple and novel method to prepare dispersed YSZ sol.•Equivalent to commercial grade.•Concentration of A-3YSZ improved up to 6 wt%.
Quisqualis indica (QI) has been used for treating disorders such as stomach pain, constipation, and digestion problem. This study was aimed to evaluate the therapeutic efficacy of QI extract on ...treating benign prostatic hyperplasia (BPH) in LNCaP human prostate cancer cell line and a testosterone-induced BPH rat model. LNCaP cells were treated with QI plus testosterone propionate (TP), and androgen receptor (AR) and prostate specific antigen (PSA) expression levels were assessed by Western blotting. To induce BPH, the rats were subjected to a daily subcutaneous injection of TP (3 mg/kg) for 4 weeks. The rats in treatment group were orally gavaged with QI (150 mg/kg) together with the TP injection. In-vitro studies showed that TP-induced increases in AR and PSA expression in LNCaP cells were reduced by QI treatment. In BPH-model rats, the prostate weight, testosterone in serum, dihydrotestosterone (DHT) concentration and 5α-reductase type 2 mRNA expression in prostate tissue were significantly reduced following the treatment with QI. TP-induced prostatic hyperplasia and the expression of proliferating cell nuclear antigen (PCNA) and cyclin D1 were significantly attenuated in QI-treated rats. In addition, QI induced apoptosis by up-regulating caspase-3 and -9 activity and decreasing the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) ratio in prostate tissues of BPH rats. Further investigation showed that TP-induced activation of AKT and glycogen synthase kinase 3β (GSK3β) was reduced by QI administration. Therefore, our findings suggest that QI attenuates the BPH state in rats through anti-proliferative and pro-apoptotic activities and might be useful in the clinical treatment of BPH.
Endoplasmic reticulum (ER) stress causes cell survival or death, which is dependent on the type of cell and stimulus. Capsaicin (8-methyl-N-vanillyl-6-nonenamide) and its analog, dihydrocapsaicin ...(DHC), induced caspase-3-independent/-dependent signaling pathways in WI38 lung epithelial fibroblast cells. Here, we describe the molecular mechanisms induced by both chemicals. Exposure to capsaicin or DHC caused induction of p53, p21, and G(0)/G(1) arrest. DHC induced massive cellular vacuolization by dilation of the ER and mitochondria. Classic ER stress inducers elicited the unfolded protein response (UPR) and up-regulation of microtubule-associated protein 1 light chain-3 (LC3) II. DHC induced ER stress by the action of heavy chain-binding protein, IRE1, Chop, eukaryotic initiation factor 2alpha, and caspase-4 and, to a lesser level, by capsaicin treatment. DHC treatment induced autophagy that was blocked by 3-methyladenine (3MA) and accumulated by bafilomycin A1. Blocking of DHC-induced autophagy by 3MA enhanced apoptotic cell death that was completely inhibited by treatment of cells with benzyl-oxcarbonyl-Val-Ala-Asp-fluoromethyl ketone. Knockdown of Ire1 down-regulated the DHC-induced Chop and LC3II and enhanced caspase-3 activation. DHC induced rapid and high-sustained c-Jun NH(2)-terminal kinase (JNK)/extracellular signal-regulated kinase (ERK) activation, but capsaicin induced transient activation of JNK/ERK. The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal. Pharmacological blockade or knockdown of ERK down-regulated LC3II. Capsaicin and DHC induced Akt phosphorylation, and the phosphatidylinositol 3-kinase inhibitors, wortmannin and LY294002 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride, induced autophagy via ERK activation. Our results indicate that the differential responses of capsaicin and DHC for cell protection are caused by the extent of the UPR and autophagy that are both regulated by the level of JNK and ERK activation.
To determine the effects of graphene oxide (GO) deposition (on a zirconia surface) on bacterial adhesion and osteoblast activation.
An atmospheric pressure plasma generator (PGS-300) was used to coat ...Ar/CH
mixed gas onto zirconia specimens (15-mm diameter × 2.5-mm thick disks) at a rate of 10 L/min and 240 V. Zirconia specimens were divided into two groups: uncoated (control; Zr) group and GO-coated (Zr-GO) group. Surface characteristics and element structures of each specimen were evaluated by field emission scanning electron microscope (FE-SEM), X-ray photoelectron spectroscopy (XPS), Raman spectroscopy, and contact angle. Additionally, crystal violet staining was performed to assess the adhesion of
. WST-8 and ALP (Alkaline phosphatase) assays were conducted to evaluate MC3T3-E1 osteoblast adhesion, proliferation, and differentiation. Statistical analysis was calculated by the Mann-Whitney
-test.
FE-SEM and Raman spectroscopy demonstrated effective GO deposition on the zirconia surface in Zr-GO. The attachment and biofilm formation of
was significantly reduced in Zr-GO compared with that of Zr (
< 0.05). While no significant differences in cell attachment of MC3T3-1 were observed, both proliferation and differentiation were increased in Zr-GO as compared with that of Zr (
< 0.05).
GO-coated zirconia inhibited the attachment of
and stimulated proliferation and differentiation of osteoblasts. Therefore, GO-coated zirconia can prevent peri-implantitis by inhibiting bacterial adhesion. Moreover, its osteogenic ability can increase bone adhesion and success rate of implants.
Endoplasmic reticulum (ER) stress has been shown to play a critical role in the pathogenesis of cardiovascular complications. However, the role and mechanisms of ER stress in hypertension remain ...unclear. Thus, we hypothesized that enhanced ER stress contributes to the maintenance of hypertension in spontaneously hypertensive rats (SHRs). Sixteen-week old male SHRs and Wistar Kyoto Rats (WKYs) were used in this study. The SHRs were treated with ER stress inhibitor (Tauroursodeoxycholic acid; TUDCA, 100 mg/kg/day) for two weeks. There was a decrease in systolic blood pressure in SHR treated with TUDCA. The pressure-induced myogenic tone was significantly increased, whereas endothelium-dependent relaxation was significantly attenuated in SHR compared with WHY. Interestingly, treatment of ER stress inhibitor normalized myogenic responses and endothelium-dependent relaxation in SHR. These data were associated with an increase in expression or phosphorylation of ER stress markers (Bip, ATF6, CHOP, IRE1, XBP1, PERK, and eIF2α) in SHRs, which were reduced by TUDCA treatment. Furthermore, phosphorylation of MLC20 was increased in SHRs, which was reduced by the treatment of TUDCA. Therefore, our results suggest that ER stress could be a potential target for hypertension.
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