• Journal of Physiology & Pathology in Korean Medicine
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• v.33 no.2
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• pp.89-101
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• 2019

In recent times, the number of men with late-onset hypogonadism has increased, and interest on this topic has also increased. This study was conducted to investigate effects of the mixture extract of Fructus amomi Amari, Eucommiae cortex, Bombyx batryticatus on improve late-onset hypogonadism. The experimental subjects consisted of three groups: a control group consisting of 8-week-old male ICR mice that had undergone no treatment, an aging-elicited group (AE group) consisting of 50-week-old ICR male mice that had undergone no treatment, and a Mixed herbal extract treatment group (MT group) consisting of 50-week-old ICR male mice that had undergone the mixture extract of Fructus amomi Amari, Eucommiae cortex, Bombyx batryticatus treatment (0.1 g/kg/day) for 6 months. After the experiment, the mice from all the experimental groups were dissected, and they were analyzed through histochemical and immunohistochemical methods. The mixture extract of Fructus amomi Amari, Eucommiae cortex, Bombyx batryticatus reduces aging-induced cell damage and oxidative stress and increases the secretion of serotonin and B-endorphin in aged mice, and promotes spermatogenesis in seminiferous tubules and reduces apoptosis and oxidative stress, and increases androgen receptor, $17{\beta}-HSD$ and GnRH, increases the ratio of smooth muscle to collagen fibers in the corpus cavernosum, increases eNOS, decreases PDE-5 and oxidative stress in aged mice, so it improves depression, reproductive, sexual problems caused by Late-onset hypogonadism. the mixture extract of Fructus amomi Amari, Eucommiae cortex, Bombyx batryticatus inhibits the induction of osteoporosis by increasing decreased bone matrix distribution due to aging, increasing the activities of OPC and OPN, which are produced in osteoblasts, and decreasing RANKL, MMP-3 activity, increasing OPG activity. It also reduces muscle damage, oxidative stress, inflammation and apoptosis of muscle tissue, and increases Myo-D in the sartorius muscle of aged mice for improving muscle atrophy caused by by Late-onset hypogonadism.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.1-9
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• 1994

It has been shown that there are several subtypes of ${\kappa}$ opioid receptor. We examined ligand binding profiles and the effects of various opioid agonists on high potassium-stimulated release of $[^3H]$ histamine. We have evaluated the properties of $non-{\mu},\;non-{\delta},$ binding of $[^3H]\;DIP\;([^3H]\;diprenorphine),$ anonselective opioid antagonist, in rat cortex membranes. Binding $to\;{\mu}\;and\;{\delta}$ sites was inhibited by the use of an excess of competing selective agonists (DAMGO, DPDPE) for these sites. (-) Ethylketocyclazocine (EKC), DIP and bremazocine inhibited $[^3H]$ DIP binding. However, arylacetamides (U69593 and U50488H) gave little inhibition Replacement of sodium by NMDG and the addition of guanine nucleotide influenced the inhibitory potency of (-) EKC, an agonist for {\kappa}_1-and-{\kappa}_2-binding site, but not of bremazocine. This result suggests that bremazocine can be an antagonist at this binding site. Also, we have examined the opioid modulation of $K^+(30mM)-induced\;[^3H]\;histamine$ release in rat frontal cortex slices labeled with $1-[^3H]\;histidine$. The $[^3H]\; histamine$ release from cortex slices was inhibited by EKC in a concentration-dependent manner. However, the ${\delta}$ receptor selective agonists, DPDPE and deltorphine II, ${\mu}$ receptor agonists, DAMGO and TAPS, ${\kappa}_1-agonists$, U69593 and U50488H, and ${\varepsilon}-agonist,\;{\beta}-endorphin,$ did not. The concentration-response curve of EKC was shifted to right in the presence of naloxone, nor-binaltorphimine and bremazocine, respectively. These results suggest that ${\kappa}_2$ opioid receptor regulates histamine release in the fromtal cortex of the rat.

• Korean Journal of Biological Psychiatry
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• v.5 no.1
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• pp.34-45
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• 1998

We provide the reader with a brief introduction to the neurobiology of neuropeptides. Several comprehensive reviews of the distribution and neurochemical, neurophysiological, neuropharmacological and behavioral effects of the major neuropeptides have recently appeared. In reviews of the large number of neuropeptides in brain and their occurance in brain regions thought to be involved in the pathogenesis of major psychiatric disorders, investigators have sought to determine whether alternations in neuropeptide systems are associated with schizophrenia, mood disorders, anxiety disorders, alcoholism and neurodegenerative disease. There is no longer any doubt that neuropeptide-containing neurons are altered in several neuropsychiatric disorders. One of the factors that has hindered neuropeptide research to a considerable extent is the lack of pharmacological agents that specifically alter the synaptic availability of neuropeptides. With the exception of naloxone and naltrexone, the opiate-receptor antagonists, there are few available neuropeptide- receptor antagonists. Two independent classes of neuropeptide-receptor antagonists has been expected to be clinically useful. Naltrexone, a potent ${\mu}$-receptor antagonist, has been used successfully to reduce the need for alcohol consumption. And cholecycstokinin antagonists are now in development as a new class of anxiolytics, which would be expected to be free from tolerance and physical dependence and lack of sedation. In this review, we deal with these two kinds of neuropeptide system, the opioid system and cholesystokinins in the brain. The role of opioid systems in the reinforcement after alcohol consumtion and that of cholesystokinins in the pathogenesis of anxiety will be discussed briefly. As we know, the future for neuropeptides in psychiatry remains bright indeed.