ABSTRACT
Background and Purpose: As it becomes an aging society, interest in senile diseases is increasing. Alzheimer's dementia (AD) and osteoporosis are representative senile diseases. Various studies have reported that AD and osteoporosis share many risk factors that affect each other's incidence. This aimed to determine if active medication treatment of AD could affect the development of osteoporosis. Methods: The Health Insurance Review and Assessment Service provided data consisting of diagnosis, demographics, prescription drug, procedures, medical materials, and healthcare resources. In this study, data of all AD patients in South Korea who were registered under the national health insurance system were obtained. The cohort underwent conversion to an Observational Medical Outcomes Partnership-Common Data Model version 5 format. Results: This study included 11,355 individuals in the good persistent group and an equal number of 11,355 individuals in the poor persistent group from the National Health Claims database for AD drug treatment. In primary analysis, the risk of osteoporosis was significantly higher in the poor persistence group than in the good persistence group (hazard ratio, 1.20 [95% confidence interval, 1.09-1.32]; p<0.001). Conclusions: We found that the good persistence group treated with anti-dementia drugs for AD was associated with a significant lower risk of osteoporosis in this nationwide study. Further studies are needed to clarify the pathophysiological link in patients with two chronic diseases.
ABSTRACT
BACKGROUND/OBJECTIVES: Male hypogonadism is a condition where the body does not produce enough testosterone and significantly impacts health. Age, obesity, genetics, and oxidative stress are some physiological factors that may contribute to testosterone deficiency. Previous studies have shown many pharmacological benefits of Schisandra chinensis (S. chinensis) Baillon as an anti-inflammatory and antioxidant. However, the molecular mechanism of attenuating hypogonadism is yet to be well established. This research was undertaken to study the effects of S. chinensis extract (SCE) on testosterone deficiency. MATERIALS/METHODS: S. chinensis fruit was pulverized and extracted using 60% aqueous ethanol. HPLC analysis was performed to analyze and quantify the lignans of the SCE. RESULTS: The 2,2-diphenyl-2-picrylhydrazyl and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) scavenging assays confirmed that the SCE and its major lignans (schisandrol A and gomisin N) inhibit oxidative stress. Effects of SCE analysis on the testosterone level under oxidative stress conditions revealed that both schisandrol A and gomisin N were able to recover the lowered testosterone levels. Through mRNA expression of TM3 Leydig cell, we observed that the SCE lignans were able to induce the enzymes involved in testosterone biosynthesis-related genes such as 3ß-HSD4 (P < 0.01 for SCE, and P < 0.001 for schisandrol A and gomisin N), 17ß-HSD3 (P < 0.001 for SCE, schisandrol A and gomisin N), and 17, 20-desmolase (P < 0.01 for schisandrol A, and P < 0.001 for SCE and gomisin N). CONCLUSIONS: These results support that SCE and its active components could be potential therapeutic agents for regulating and increasing testosterone production.
ABSTRACT
Inflammatory responses are involved in various diseases, such as insulin resistance, atherosclerosis, and hypogonadism. This study investigates the effects of SCE on anti-inflammation and molecular mechanisms in LPS-induced macrophages. RAW 264.7 macrophage cells were treated with LPS for 24 hr, followed by SCE, schisandrin C (Sch C) (1, 10, and 100 µM), and gomisin N (GN) (1, 10, and 100 µM) for 24 hr. Gene expression levels of pro-inflammatory cytokines were measured by qPCR. Protein expression of NLPR3 inflammasome was examined by western blot analysis. The expression levels of pro-inflammatory cytokines, including IL-1ß, IL-6, and TNFα, were significantly reduced after SCE treatment. Sch C significantly inhibits these pro-inflammatory cytokines, while GN suppresses only IL6. Furthermore, Sch C significantly prevented the activation of NLRP3 inflammasome complexes such as NLRP3 and caspase-1. Sch C is the major active compound of SCE on anti-inflammation through attenuation of NLRP3 inflammasome.
