Background: Polycystic ovary syndrome (PCOS) is an oxidative state resulting in ovarian dysfunction. Licorice is one of the natural antioxidants used for the treatment of infertility.
Objective: To evaluate the effect of licorice extract on ovarian morphology, oocyte maturation, and embryo development in PCOS-induced mice.
Materials and Methods: thirty-two female NMIR mice were divided into four groups (n = 8/each): control group receiving no treatment (group I); PCOS group injected with estradiol valerate once daily for 21 days (group II); and experimental groups receiving either 100 mg/kg (group III) or 150 mg/kg (group IV) licorice by gavage along with estradiol valerate once daily for 3 wk. Serum levels of the testosterone and estrogen were measured using ELISA kit. Histological study of ovaries was evaluated, and oocyte maturation, fertilization rate, and embryo development were determined after in vitro maturation.
Results: Experimental groups (III, IV) had significantly higher testosterone and estradiol levels compared to the PCOS group (p ≤ 0.001). A significant increase in the number of healthy follicles (primary, preantral follicles) (p = 0.001), corpus luteum (p = 0.001) with significant decrease in the number of atretic follicles (primary, preantral, cystic follicles) (p ≤ 0.001) was seen in the experimental groups. Increase in the fertilization rate (p ≤ 0.001) and blastocyst stage embryos (p = 0.02, p = 0.004) were observed in the experimental groups.
Conclusions: It appears that the two doses (100 mg and 150 mg) of licorice could decrease ovarian cyst and improve the fertilization rate of oocyte and embryo development in PCOS mice. However, there was no statistically significant difference between the two experimental groups.
Key words: Polycystic ovary syndrome, Mice, Licorice, Histology, In vitro maturation, In vitro fertilization.
The applications of 3D bioprinting are becoming more commonplace. Since the advent of tissue engineering, bone has received much attention for the ability to engineer normal bone for tissue engraftment or replacement. While there are still debates on what materials comprise the most durable and natural replacement of normal tissue, little attention is given to recreating diseased states within the bone. With a better understanding of the cellular pathophysiology associated with the more common bone diseases, these diseases can be scaled down to a more throughput way to test therapies that can reverse the cellular pathophysiology. In this review, we will discuss the potential of 3D bioprinting of bone tissue in the following disease states: osteoporosis, Paget’s disease, heterotopic ossification, osteosarcoma, osteogenesis imperfecta, and rickets disease. The development of these 3D bioprinted models will allow for the advancement of novel therapy testing resulting in possible relief to these chronic diseases.
Rheumatoid arthritis (RA) is a chronic inflammatory condition of synovial joints that causes disability and systemic complications. Ang-(1-7), one of the main peptides in the renin-angiotensin (Ang) system (RAS), imposes its protective effects through Mas receptor (MasR) signaling. It has a short half-life, limiting its feasibility as a therapeutic agent. In this study, we evaluated the anti-inflammatory effects of Ang-(1-7)’s novel and stable conjugate (Ang. Conj.) by utilizing its affinity for bone through bisphosphonate (BP) moiety in an adjuvant-induced arthritis (AIA) rat model. The rats received subcutaneous injections of vehicle, plain Ang-(1-7), or an equivalent dose of Ang. Conj. The rats’ body weights, paws, and joints’ diameters were measured thrice weekly. After 14 days, the rats were euthanized, and the blood and tissue samples were harvested for further analysis of nitric oxide (NO) and RAS components’ gene and protein expression. The administration of Ang. Conj. reduced body weight loss, joint edema, and serum NO. Moreover, the Ang. Conj. treatment significantly reduced the classical arm components at peptide, enzyme, and receptor levels while augmenting them for the protective arm. The results of this study introduce a novel class of bone-targeting natural peptides for RA caused by an inflammation-induced imbalance in the activated RAS. Our results indicate that extending the half-life of Ang-(1-7) augments the RAS protective arm and exerts enhanced therapeutic effects in the AIA model in rats.
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