[This corrects the article DOI 10.2147/DDDT.S46323.].
The aim of the present study was to evaluate the expression of inflammasome and cytokine on experimental periodontitis with super activated platelet lysate (SPL) in rats.
Periodontitis was induced by submerging cotton ligatures on the right side of the maxillary second molar in 36 Wistar rats. The rats were divided into 3 groups randomly the rats received no treatment (control group); local injection with sterile saline (ligature+saline group) and local injection with SPL (ligature+SPL group). After treatments, the alveolar bone level and inflammation of periodontal tissue were evaluated by micro-computed tomography (micro-CT) scanning and histological examination, respectively. The expression of inflammasome and cytokine was evaluated by real-time quantitative polymerase chain reaction (RT-qPCR) assay.
Compared with the control group, the bone loss significantly increased by 0.9 mm in the ligature+saline group and 0.4 mm in the ligature+SPL group (P < 0.001). 0.5 mm reduction in the bone loss was founded in the ligature+SPL group compared with the ligature+saline group (P < 0.001). The gene expression of
was significantly reduced in the ligature+SPL group compared with the ligature+saline group (P < 0.05). Compared with the ligature+saline group, the expression for inflammasome
was both downregulated in the ligature+SPL group (P < 0.05).
Our present study demonstrated local injection of SPL regulated the expression of inflammasome and cytokine and had a visible effect of relieving inflammation in the experimental periodontitis in rats.
Our present study demonstrated local injection of SPL regulated the expression of inflammasome and cytokine and had a visible effect of relieving inflammation in the experimental periodontitis in rats.
Osteoarthritis (OA) is a prevalent articular disorder and has no entirely satisfactory treatment. Punicalagin (PUG) is a polyphenol which has shown multiple pharmacological effects on various diseases. However, the role of PUG in the treatment of OA has not been well defined.
The effects of PUG on anti-oxidative stress, anti-apoptosis, extracellular matrix (ECM) degradation and autophagy were evaluated in chondrocytes through Western blot and immunofluorescence (IF) staining. Meanwhile, the effects of PUG on destabilization of the medial meniscus (DMM) model were also assessed in vivo by performing histopathologic analysis and IF staining.
In vitro, PUG treatment not only increased the level of HO-1 and SOD1 against oxidative stress but also suppressed the expression of apoptotic proteins and inhibited ECM degradation. Meanwhile, PUG treatment activated autophagy and restores autophagic flux in chondrocytes after tert-butyl hydroperoxide (TBHP) insult, inhibition of autophagy by 3-methyladenine (3-MA) partly abrogated the protective effects of PUG on chondrocytes. In vivo, degeneration of the articular cartilage following DMM was also ameliorated by PUG treatment.
PUG prevents the progression of OA through inhibition of apoptosis, oxidative stress and ECM degradation in chondrocytes, which mediated by the activation of autophagy.
PUG prevents the progression of OA through inhibition of apoptosis, oxidative stress and ECM degradation in chondrocytes, which mediated by the activation of autophagy.
We aimed to investigate the effect of switching from tenofovir disoproxil fumarate (TDF) to tenofovir alafenamide (TAF) on the hepatic safety and metabolic profile.
Consecutive HIV patients, enrolled in the Surveillance Cohort Long-term Toxicity Antiretrovirals/Antivirals (SCOLTA) project, switching from TDF to TAF were included. Changes from baseline (T0) to 6-month follow-up (T1) were evaluated using paired
-test and signed rank test.
A total of 190 patients switched from TDF to TAF and had one 6-month follow-up visit. They were 80% male, 74.2% at CDC stage A-B, 93.7% with undetectable HIV-viral load. Mean age was 46.7±10.7 years, body mass index was 25.0±3.9 kg/m
, median CD4 cell count was 634 cell/µL (interquartile range [IQR]=439-900), aspartate aminotransferase (AST) was 23 (IQR=19-30) IU/L, and alanine aminotransferase (ALT) was 24 (IQR=17-34) IU/L. At T1, both AST (median=-1, IQR=-5-2 IU/L,
=0.004) and ALT (median=-2, IQR=-7-3 IU/L,
=0.0004) showed a significant decrease. Among 28 patients with ALT >40 at baseline, reduction was significant both clinically (-17, IQR=-32--1) and statistically (
=0.0003). Total cholesterol levels (TC) increased (+13.4±3.8 mg/dL,
=0.0006), as well as HDL-cholesterol (HDL-C) (+3.8±1.2 mg/dL,
=0.02), LDL Cholesterol (LDL-C) (+7.6±3.4,
=0.03) and glucose (+4.0±1.8 mg/dL,
=0.02). DAD and Framingham risk score did not change at 6 months after switch.
A significant reduction of liver enzymes was observed after switching from TDF to TAF, especially in subjects with initial level of ALT >40 IU/L. Plicamycin Glucose, TC, HDL-C, and LDL-C increased, with no effect on cardiovascular risk scores.
40 IU/L. Glucose, TC, HDL-C, and LDL-C increased, with no effect on cardiovascular risk scores.
To describe the anatomical and functional results of the implantation of asymmetric thickness intracorneal ring segments (AS-ICRS) in eyes with keratoconus and asymmetric/irregular astigmatism (type 2 -
and type 3 -
phenotypes, Fernandez-Vega/Alfonso morphologic Keratoconus classification).
Retrospective observational study including 19 consecutive patients (21 eyes) with keratoconus who underwent manual implantation of the Keraring
Asymmetric ICRS (AS). Analysis included demographic and clinical data and Pentacam (Oculus
) measurements topographic astigmatism; topographic flat meridian (K1), steepest meridian (K2) and the maximum keratometric point (Kmax); total root mean square (RMS) and high order RMS (HOA) aberrations and comatic Zernike coefficients (Z3
;Z3
) at 0º and 90º meridians.
Overall mean age was 35.3±11.7 years and median follow-up was 7.1 months (range 6-12). At the end of follow-up, a significant improvement from baseline was achieved in both UDVA (0.24±0.22; p=0.017) and CDVA (0.Plicamycin
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