Intervention Research Of Phenylethyl Alcohol GlycosidesinCistanche On Perimenopausal Syndrome Animal Model

Abstract Objective: To observe the influence of Phenylethyl alcohol glycosideside of Cistanche to the menopausal transition of rat and mouse, perimenopausal depression models of rat, and to explore the Phenylethyl alcohol glycosideside Cistanche in the treatment of perimenopausal syndrome and its characteristics. 

Methods: The menopausal transition model of rats was established by the method of back bilateral sides to remove the complete ovary. After administration for 21days, the number of independent activities, the incubation period of the first to enter a darkroom, electric times were determined, moist Uterus, thymus and spleen were weighed to calculate the viscera index, serum estradiol (E2), testosterone (T) and luteinizing hormone (LH), follicle-stimulating hormone (FSH) levels were detected,thenmicethymus, spleen, uterus, pituitary gland, the hypothalamus. The menopausal transition mouse was established by the back single side to remove the completely and the back other side to remove the ovary for 80%. After administration for 30days, levels - vertical movement of integral was determined, moist Uterus, thymus andspleenwere weighed to calculate the viscera index, estradiol (E2), testosterone (T), luteinizing hormone (LH), follicle-stimulating hormone (FSH), gonadotrophin-releasing hormone (GnRH), the content of osteocalcin (BGP) in serum, Plasma beta-endorphin (betaEP), the hypothalamus, pituitary, uterus tissue homogenate, the content of ERinthehypothalamus, and AR in the tissue homogenate were determined. The menopausal transition model of rats was established by the method of back bilateral sides to remove completely ovary combined with chronic stimulation. After administration for 30 days, the number of independent activities for 5 minutes, the incubation period of the first to enter a dark room, electric times for 5 minutes, the fixed time of forced swimming and tail suspension test in mice within 6 min 2 ~ 6 minutes was determined, moistUterus, thymus, and spleen were weighed to calculate the viscera index. Braintissuehomogenate of serotonin (5 - HT) and the content of dopamine (DA) was determined, and levels of serum estradiol (E2), testosterone (T), and luteinizing hormone(LH), follicle-stimulating hormone (FSH) were detected Results: The menopausal transition model of the rat was established successfully. The number of autonomic activities in the mice model group was significantly reduced, in avoiddark experiments first time in a dark room during the incubation period. Times of Shock by electricity rose significantly, levels of serum E2 and T significantly decreased, and levels of serum FSH, and LH increased significantly. The thymus, spleen, and uterus index dropped significantly. Phenethyl alcohol glycoside can increase the activity of the menopausal transition model mice, and memory, and can improve the thymus, spleen, uterus index, and the level of serum E2, T, lower levels of serum FSH, LH. The menopausal transition model of the mouse was established successfully.Level of model group rats - vertical movement points dropped significantly, serumE2, T, significantly reduced, level of serum FSH, LH, and GnRH significantly increased, levels of β-EP in plasma decreased; the level of AR and ER in the hypothalamus, pituitary, uterus significantly declined, thymus, spleen, uterus index dropped significantly.phenethyl alcohol glycoside can increase the activity of the menopausal transition model rats, enhance the uterus, thymus, and spleen index and serumE2, T, BGP, level of plasmaβ-EP, the hypothalamus of AR and ER level in the hypothalamus, pituitary, uterus, lowered levels of serum FSH, LH, GnRH. The perimenopausal depression model of mice was established, The Model group mice forced swimming, and tail suspension fixedtimeincreased, the number of independent activities reduced, dark experiments in a darkroom for the first time the incubation period reduced, power frequency increased, the level of serum E2, T was decreased significantly, levels of serum FSH, LHincreasedsignificantly, levels of the brain 5 - HT, DA, thymus, spleen, the uterus of viscera index decreased.Phenylethyl alcohol glycosides could increase the activity of perimenopausal depression model mice, enhance memory in mice and prolong the incubation period, decrease The Times of the mice forced swimming, and tail suspension fixed times reduced, can make the uterus, thymus, and spleen index and the serum level of E2, T, the brain 5 - HT and DA content increased, reduced serum FSH, LH levels. Conclusion: Each dose of phenethyl alcohol glycoside in Cistanche cannot only against the sex hormone (E2, T, FSH, LH) disorder of perimenopausal syndrome but also adjust the level of sex hormone receptor (ER, AR) disorders, improve the body's immune function, correct state of osteoporosis, increase the uterus, thymus, spleen index. 

Keywords: perimenopausal syndrome; Perimenopausal depression; Cistanche; phenyl ethyl alcohol glycosides; menopausal transition animal model

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Introduction Perimenopausal syndrome is a syndrome mainly caused by autonomic nervous system dysfunction caused by estrogen secretion disorder and is accompanied by neuropsychological symptoms. Symptoms include varying degrees of hot flashes and sweating, irritability, dizziness, tinnitus, Heart palpitations, insomnia, etc. In the late stages, osteoporosis, memory loss, cognitive decline, cardiovascular and cerebrovascular diseases, etc. can be seen. The main reason is that ovarian function gradually declines and disappears, which occurs before and after menopause. Therefore, traditional Chinese medicine calls it "pre- and post-menopausal diseases". "Cards", "Cards before and after menstruation".

Modern clinical medicine believes that estrogen receptors are widely present in many tissues and organs throughout the body. Ovarian function decreases, estrogen secretion decreases, and its target tissues and organs produce a series of functional and histomorphological changes, causing perimenopausal syndrome. Decreased estrogen levels are the basis of perimenopausal syndrome. However, scholars have found that perimenopausal syndrome is also accompanied by changes in neurotransmitters, changes in immune function, changes in free radicals, and cell apoptosis. In recent years, theories such as endocrine, neurotransmitters, immunity, free radicals, and apoptosis have emerged, among which research is mainly conducted around the endocrine theory [1]. Basedovsky used the famous neuroendocrine-immune network theory to connect the three systems of endocrine theory, neurotransmitter theory, and immune theory, which were considered to perform their duties in the past, into a complete network system. This is the transformation of modern medicine from a local perspective to a holistic perspective. a major development and progress. Many scholars have studied the treatment mechanism of perimenopausal syndrome, mainly focusing on the endocrine system, nervous system, immune system, and other aspects of the body.

The endocrine theory holds that gonadotropin-releasing hormone (GnRH) secreted by the hypothalamus promotes the secretion of two gonadotropins by the anterior pituitary gland - follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which promote ovarian production and secretion of estrogen. Hormones and progesterone, the estrogen and progesterone secreted by the ovary, and the gonadotropins secreted by the pituitary gland have a feedback regulatory effect on the synthesis, secretion, and release of hormones related to the hypothalamus and pituitary gland. The hypothalamus-pituitary-ovary axis The interaction keeps female reproductive endocrine relatively stable [2]. In the same way, the balance of the hypothalamus-pituitary-ovary axis (gonadal axis) is imbalanced, the secretion of sex hormones in the reproductive endocrine system is disordered, the ovary's ability to stress gonadotropins is weakened, and the secretion of estrogen is greatly reduced, which causes feedback in the hypothalamus, Hypersecretion of the pituitary gland and excessive secretion of gonadotropin cause autonomic nervous system dysfunction, leading to hot flashes, sweating, irritability, insomnia and other symptoms of autonomic nervous system disorders [3].

The neurotransmitter theory believes that decreased estrogen levels lead to changes in the secretion of neurotransmitters in the hypothalamic limbic system, especially imbalances in the secretion of 5-hydroxytryptamine, dopamine, etc. DA is an important neurotransmitter in the extrapyramidal system, which is closely related to body motor function and can also affect people's emotional activity and general behavior [4]. There are receptors (ER) in the β-EP neurons of the arcuate nucleus of the hypothalamus, and the release and activity of hypothalamic β-EP decrease during perimenopause [5]. The immune theory holds that when the levels of estrogen (E2) and testosterone (T) in the body decrease excessively, immune active cells cannot receive physiological doses of estrogen stimulation, estrogen receptors decrease accordingly, and the biological effects of estrogen and its receptors decrease. Subsequently, immune active cells cannot effectively produce sufficient immune mediators, and the ratio of norepinephrine (NE) is imbalanced, leading to PMS [6]. After menopause, with the gradual loss of ovarian function, the levels of estrogen and androgens decrease, mainly the levels of estradiol (E2) and testosterone (T). The decrease in estrogen levels reduces the negative feedback regulation of the hypothalamus and pituitary gland, GnRH, The levels of LH and FSH increase, and the central neurotransmitter substance P increases. Hypothalamic β-EP is a peptide substance that can effectively inhibit the release of GnRH. The decrease in the release and activity of β-EP leads to an increase in the NE/DA ratio. , causing hot flashes [7]. Reduced T levels will affect the bone structure, muscle mass, and cardiovascular system, and is one of the signs of osteoporosis in women; T plays an important role in maintaining estrogen synthesis, and abnormal androgen levels are also a predisposing factor for PMS [8];3

The neurotransmitter theory believes that decreased estrogen levels lead to changes in the secretion of neurotransmitters in the hypothalamic limbic system, especially imbalances in the secretion of 5-hydroxytryptamine, dopamine, etc. DA is an important neurotransmitter in the extrapyramidal system, which is closely related to body motor function and can also affect people's emotional activity and general behavior [4]. There are receptors (ER) in the β-EP neurons of the arcuate nucleus of the hypothalamus, and the release and activity of hypothalamic β-EP decrease during perimenopause [5]. The immune theory holds that when the levels of estrogen (E2) and testosterone (T) in the body decrease excessively, immune active cells cannot receive physiological doses of estrogen stimulation, estrogen receptors decrease accordingly, and the biological effects of estrogen and its receptors decrease. Subsequently, immune active cells cannot effectively produce sufficient immune mediators, and the ratio of norepinephrine (NE) is imbalanced, leading to PMS [6]. After menopause, with the gradual loss of ovarian function, the levels of estrogen and androgens decrease, mainly the levels of estradiol (E2) and testosterone (T). The decrease in estrogen levels reduces the negative feedback regulation of the hypothalamus and pituitary gland, GnRH, The levels of LH and FSH increase, and the central neurotransmitter substance P increases. Hypothalamic β-EP is a peptide substance that can effectively inhibit the release of GnRH. The decrease in the release and activity of β-EP leads to an increase in the NE/DA ratio. , causing hot flashes [7]. Reduced T levels will affect the bone structure, muscle mass, and cardiovascular system, and is one of the signs of osteoporosis in women; T plays an important role in maintaining estrogen synthesis, and abnormal androgen levels are also a predisposing factor for PMS [8];

The withdrawal of sex hormones caused by menopause results in a decrease in the monoamine neurotransmitters dopamine (DA) and 5-hydroxytryptamine (5-HT) in the brain [9]. Estrogen can increase 5-HT and DA, thereby improving patients' emotional responses and memory. Various human hypothalamic neurons (including β-endorphin and dopamine neurons) and pituitary gonadotropin cells contain estrogen receptors (ER) and androgen receptors (AR) and therefore can respond to the feedback effects of sex hormones. , sex hormones can regulate the release of GnRH by modifying GnRH gene transcription and regulating neurotransmitter activity [10]. For women during menstruation, the decrease in immunity is related to the decrease in E2 levels. The increase in serum E2 can increase the content of β-EP secreted by the hypothalamus and enhance immunity. This shows that the increase in the biological effect of estrogen is due to the increase in β-EP content. Reasons for enhanced immunity[11]. The improvement of immune function has a positive impact on hormones, neurotransmitters, etc., stabilizing the internal environment of the body. In addition, estrogen directly acts on the ER on osteoblasts to affect the synthesis and expression of BGP. The above theories each have their characteristics and overlap with each other, but estrogen level disorders run through the three theories. HPO axis disorder is the fundamental cause of PMS, and an imbalance of estrogen and androgen levels is an important manifestation of the disorder; currently, hormone replacement therapy (HRT) directly supplements the reduced estrogen and is the main therapy to prevent and treat this disease (including estrogen therapy alone, estrogen therapy alone, and estrogen therapy alone). Combined use of hormones and progestins, combined use of estrogen and androgens, combined use of three hormones, single use of progestins, etc.). However, since hormone therapy has its indications, strict contraindications, and caution, various indicators must be actively monitored and checked regularly during hormone therapy. Long-term estrogen replacement therapy can cause adverse effects such as vaginal bleeding, breast tenderness, endometrial cancer, and breast cancer. In addition to the unsatisfactory efficacy of using estrogen to treat patients with menopausal syndrome, medicinal doses of estrogen still have a suppressive effect on the immune system.

[12]. Especially the recent discovery that it can increase the occurrence of serious side effects such as cardiovascular and cerebrovascular risks has limited the clinical application of this method.

Cistanche Y.C.Ma is a perennial parasitic medicinal plant belonging to the Cistanche family. It has the functions of nourishing kidney yang, replenishing essence, and blood, moistening the intestines, and being laxative. Modern research shows that it has the effects of anti-aging, enhancing human immunity, enhancing memory and learning ability, anti-inflammation, and anti-fatigue [17]. Cistanche is a commonly used kidney-tonifying and yang-improving drug in traditional Chinese medicine, and is known as "desert ginseng". The main medicinal components of Cistanche , phenylethanoid glycosides, have androgen-like effects, which is the embodiment of modern medicine in tonifying kidney yang [18]. Perimenopausal syndrome is mainly due to the decline of ovarian function and a decrease in estrogen secretion, which causes endocrine disorders, low immunity, and autonomic nervous system disorders, leading to dysfunction and pathological changes in multiple systems throughout the body. To explore the relationship between sex hormone levels, kidney function, and improvement of perimenopausal syndrome symptoms and perimenopause, to provide a new idea and method for the treatment of female perimenopausal syndrome and other related diseases, and to study the prevention and treatment of perimenopausal syndrome. It provides a basis for new traditional Chinese medicines to treat symptoms, and can also further explore the pathogenesis and characteristics of perimenopausal syndrome. Further, improve and enrich the theory of "counter-control and adjustment of balance". This study uses the completely castrated mouse perimenopausal syndrome model, the incompletely castrated mouse perimenopausal syndrome model, and the complete castrated mouse combined with chronic unpredictable stress to create a mouse perimenopausal depression model as the research subjects. Study on the characteristics and mechanism of Cistanche phenylethanol glycoside in the treatment of female perimenopausal syndrome through the effects of Cistanche phenylethanol glycoside on the levels of intuitive indicators E2, T, FSH, and LH, which are the direct cause of perimenopausal syndrome. Syndrome tissue changes are the direct result of excessive decreases in estrogen and androgen levels. The perimenopausal syndrome can lead to hypothalamic-pituitary-gonadal axis (HPO) dysfunction. To explore the changes in estrogen levels in the body and the characteristics of drug effects, we Corresponding indicators were also systematically tested and analyzed. Serum GnRH and BGP levels, plasma β-EP levels, and the production of biological effects of estrogen and androgens were closely related to the content of receptors in relevant tissues. The levels of estrogen and androgen receptors in relevant tissues were also detected. content; perimenopausal depression can also affect the imbalance of monoamine neurotransmitters in the hypothalamus. This study will also observe the impact on 5-HT and DA levels. Through the above studies, the mechanism and characteristics of Cistanche phenylethanol glycoside in the treatment of perimenopausal syndrome are revealed from the perspective of estrogen and male hormone and receptor levels and HPO function; the research on the active parts of Cistanche , a kidney-tonifying and Yang-tonifying drug, in the treatment of female perimenopausal syndrome is being discussed. In addition to the action characteristics of Cistanche phenylethanol glycoside, it can also provide new ideas and methods for the treatment of female perimenopausal syndrome.

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