1.Neuroprotective effect of caffeic acid phenethyl ester in 3-nitropropionic acid-induced striatal neurotoxicity.
Jia BAK ; Hee Jung KIM ; Seong Yun KIM ; Yun Sik CHOI
The Korean Journal of Physiology and Pharmacology 2016;20(3):279-286
Caffeic acid phenethyl ester (CAPE), derived from honeybee hives, is a bioactive compound with strong antioxidant activity. This study was designed to test the neuroprotective effect of CAPE in 3-nitropropionic acid (3NP)-induced striatal neurotoxicity, a chemical model of Huntington's disease (HD). Initially, to test CAPE's antioxidant activity, a 2,2'-azino-bis-3-ethylbenzthiazoline-6-sulfonic acid (ABTS) antioxidant assay was employed, and CAPE showed a strong direct radical-scavenging eff ect. In addition, CAPE provided protection from 3NP-induced neuronal cell death in cultured striatal neurons. Based on these observations, the in vivo therapeutic potential of CAPE in 3NP-induced HD was tested. For this purpose, male C57BL/6 mice were repeatedly given 3NP to induce HD-like pathogenesis, and 30 mg/kg of CAPE or vehicle (5% dimethyl sulfoxide and 95% peanut oil) was administered daily. CAPE did not cause changes in body weight, but it reduced mortality by 29%. In addition, compared to the vehicle-treated group, robustly reduced striatal damage was observed in the CAPE-treated animals, and the 3NP-induced behavioral defi cits on the rotarod test were signifi cantly rescued after the CAPE treatment. Furthermore, immunohistochemical data showed that immunoreactivity to glial fibrillary acidic protein (GFAP) and CD45, markers for astrocyte and microglia activation, respectively, were strikingly reduced. Combined, these data unequivocally indicate that CAPE has a strong antioxidant eff ect and can be used as a potential therapeutic agent against HD.
Animals
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Astrocytes
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Body Weight
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Cell Death
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Dimethyl Sulfoxide
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Glial Fibrillary Acidic Protein
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Humans
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Huntington Disease
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Male
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Mice
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Microglia
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Models, Chemical
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Mortality
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Neurons
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Neuroprotective Agents*
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Rotarod Performance Test
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Urticaria
2.Clinics in diagnostic imaging (202). Osgood-Schlatter disease (OSD).
Jeremy Jia Hong LAM ; Sandeep Halagatti VENKATESH ; Chi Long HO ; Bak Siew Steven WONG
Singapore medical journal 2019;60(12):610-615
A 14-year-old boy presented with left anterior knee pain, which was aggravated by exercise and relieved by rest. On clinical examination, there was tenderness at the tibial tuberosity with reproducible pain on resisted active extension of the knee. Radiographs showed heterotopic ossification of the patellar tendon with irregularity and fragmentation of the tibial tubercle. Clinical and radiological findings were consistent with Osgood-Schlatter disease, which is a traction apophysitis of the tibial tubercle commonly occurring in adolescents. The clinical presentation and imaging features are discussed.
3.Schisandrol A and gomisin N from Schisandra chinensis extract improve hypogonadism via anti-oxidative stress in TM3 Leydig cells
Jia BAK ; Seung Ju LEE ; Tae Won KIM ; Seonhwa HWANG ; Min Ju PARK ; Rohith ARUNACHALAM ; Eunsoo YOO ; Min Hi PARK ; Yun-Sik CHOI ; Hye Kyung KIM
Nutrition Research and Practice 2023;17(1):1-12
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 3β-HSD4 (P < 0.01 for SCE, and P < 0.001 for schisandrol A and gomisin N), 17β-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.