Evaluation of the Shear Bond Strength and Antibacterial Activity of Orthodontic Adhesive Containing Silver Nanoparticle, an In-Vitro Study.

This study evaluated the effect of incorporating silver nanoparticles (AgNPs) into conventional orthodontic adhesive on its antibacterial activity and the shear bond strength (SBS) to stainless steel orthodontic brackets. Thirty-four extracted premolars were randomly allocated into two groups (n = 17). Orthodontic adhesive (Transbond XT, 3M Unitek) was blended with AgNPs (50 nm, 0.3% w/w) to form a nano-adhesive. In order to bond stainless steel twin brackets (0.022-inch, American Orthodontics), Transbond XT (n = 17) and nano-adhesive (n = 17) were used in each group, respectively, after acid etching (37% phosphoric acid, 30 s) and rinsing with water (15 s). SBS and the adhesive remnant index (ARI) scores were recorded. Antibacterial activity against Streptococcus mutans in both groups after 24 h and 30 days was assessed (Disc agar diffusion test) and the inhibition zone diameter around each specimen was measured and recorded. Adding AgNPs significantly (p = 0.009) reduced the mean (SD) SBS in the nano-adhesive group [10.51(7.15) MPa] compared to Transbond XT [17.72(10.55) MPa]. The ARI scores on the Transbond XT and nano-adhesive showed no statistically significant difference (p = 0.322). Nano-adhesive with AgNPs showed significant antibacterial activity against Streptococcus mutans at 24 h and 30 days (p < 0.001). In both groups, no significant decline in the zones of inhibition was detected after 30 days (p = 0.907). The findings suggest that SBS decreased after incorporation of AgNPs [0.3% (w/w)], but was still above the recommended SBS of 5.9-7.8 MPa. The nano-adhesive showed significant antibacterial activity which did not change much after 30 days.

Dual targeting of TNF-α and free radical toxic stress as a promising strategy to manage experimental polycystic ovary.

CONTEXT: It is now clear that oxidative stress (OS) and chronic low-grade inflammation are two main pathways involved in polycystic ovary syndrome (PCOS) pathogenesis. Therefore, simultaneous targeting of these pathways by means of carvedilol and Semelil (ANGIPARS™), as established medicines with dual anti-cytokine and anti-oxidant potential may be a therapeutic alternative approach to the current treatments. OBJECTIVE: The objective of this study is to study the protective effects of carvedilol and ANGIPARS™ on inflammatory and oxidative response in hyperandrogenism-induced polycystic ovary (PCO). MATERIALS AND METHODS: The murine model of PCO was induced by letrozole (1 mg/kg/d; orally) and effective doses of carvedilol (10 mg/kg/d; orally) and ANGIPARS™ (2.1 mg/kg/d; orally) were administrated for 21 d in PCO and non-PCO healthy rats. Ovarian folliculogenesis, sex hormones concentrations, OS, inflammatory, and metabolic biomarkers were assessed in serum and ovaries. RESULTS: PCO rats exhibited ovarian cystogenesis which was preserved by the application of carvedilol and ANGIPARS™. In comparison with controls, decreased level of the total antioxidant power (TAP) and higher levels of reactive oxygen species (ROS) and lipid peroxidation (LPO) in serum and ovaries (2.41 ± 0.67 versus 0.72 ± 0.11; and 0.17 ± 0.04 versus 0.05 ± 0.01; 5.48 ± 1.30 versus 10.56 ± 0.77; and 7.06 ± 1.94 versus 17.98 ± 0.98; p < 0.05, respectively) were detected in PCO rats. Moreover, the PCO rats exhibited hyperandrogenism due to a 3.7-fold increase in serum testosterone concentration (35.04 ± 3.17 versus 131.09 ± 13.24; p < 0.05) along with a 2.98-fold decrease in serum progesterone (6.19 ± 0.40 versus 18.50 ± 1.03; p < 0.05) and 5.2-fold decrease in serum estradiol (9.30 ± 0.61 versus 48.3 ± 2.10; p < 0.05) when compared with those of the control group. However, similar to the control group, normal levels of OS markers and sex hormones were detected in ANGIPARS™ and carvedilol co-treated PCO rats. Besides, when compared with controls, increased levels of TNF-α (770.75 ± 42.06 versus 477.14 ± 28.77; p < 0.05) and insulin (1.27 ± 0.10 versus 0.36 ± 0.05; p < 0.05) in PCO rats were significantly inhibited by carvedilol and ANGIPARS™ co-treatment. DISCUSSION AND CONCLUSION: We evidenced the beneficial effects of carvedilol and ANGIPARS™ in PCO, which underpin the new alternative approach in using these kinds of medicines in female reproductive disorders.

Cellular and molecular mechanisms of pentoxifylline's beneficial effects in experimental polycystic ovary.

Chronic low-grade inflammation and oxidative stress (OS) appear to be two main pathways involved in the pathogenesis of polycystic ovary (PCO) syndrome. Therefore, targeting these pathways by means of anticytokine and antioxidant agents might be a therapeutic alternative approach to the current treatments of PCO syndrome. In this study, we investigated the protective effects of pentoxifylline (PTX), a drug with antioxidant and anti-tumor necrosis factor alpha (TNF-α) properties, in hyperandrogenism-induced PCO rats. The inflammatory and OS responses and their connections with ovarian functionality in induced PCO rats were investigated through ovarian histopathologic examination and a series of biochemical measurements including serum estradiol, progesterone, testosterone, insulin, and TNF-α, ovarian and serum lipid peroxidation, total antioxidant power, and reactive oxygen species. Experimental PCO was induced in rats by oral administration of letrozole (1 mg/kg body weight) for 21 consecutive days. In a different group, PTX was administrated orally (50 mg/kg/d) for 21 days simultaneous with letrozole to assess its potential protective effects. The letrozole-induced PCOs were characterized by irregular cycles, high incidence of subcapsular ovarian cysts with diminished or scant granulosa cell layers, increased number of atretic preantral and antral follicles, and absence of CL. In addition, the letrozole-induced PCO rats exhibited notable increase in lipid peroxidation and reactive oxygen species of serum and ovary, serum testosterone, insulin, and TNF-α and significant decline in total antioxidant power, serum estradiol, and serum progesterone. Our results indicated that all the identified pathologic parameters and biochemical characteristics in letrozole-induced PCO rats in this study were preserved close to normal levels by simultaneous PTX treatments. Present results demonstrate that there is a direct connection between ovarian dysfunction and increased OS and inflammation in PCO. For the first time, the beneficial effects of PTX as a powerful antioxidant and TNF-α blocker in hyperandrogenism-induced PCO are reported.