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SUMMARY OBJECTIVE: Gastric cancer ranks the third among the cancer-related deaths. It is diagnosed at advanced stage in many patients due to malignant proliferation and has a poor prognosis. Currently, no instrument or biomarker has been proven to diagnose the disease before the advanced stages. This study aimed to measure the serum levels of galanin and obestatin, which were examined in various studies including cancer studies, and to discuss their diagnostic value in gastric cancers. METHODS: In this study, 30 adult patients with gastric cancer and 30 healthy adults in the control group were examined prospectively. The demographic characteristics and serum levels of galanin and obestatin in the patient and control groups were recorded. RESULTS: The mean serum level of galanin in the patient and control groups was 19.73±5.04 and 35.59±10.94 pg/mL, respectively. The mean serum level of obestatin in the patient and control groups was 40.21±5.82 and 15.15±3.32 ng/mL, respectively. A significant difference was found between the groups (p<0.001). CONCLUSION: Serum levels of galanin were lower and serum levels of obestatin were higher in patients with gastric cancer compared to the healthy individuals. Serum levels of obestatin and galanin can be used as potential biomarkers in the diagnosis of gastric cancer.
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ABSTRACT Objective: Galanin is a neuropeptide which has effects not only on metabolic syndrome but also on reproduction. Glypican-4 is an adipokine associated with insulin sensitivity by interacting directly with the insulin receptor. This study evaluated serum concentrations of galanin and glypican-4 in relation with the hormonal profile as well as metabolic and cardiovascular risk factors in patients with and without polycystic ovary syndrome (PCOS). Subjects and methods: A total of 44 women with PCOS and 44 age-matched controls were eligible. Hirsutism scores, hormonal profile, metabolic and cardiovascular risk factors as well as galanin and glypican-4 levels were evaluated in each subject. Results: Women with PCOS exhibited lower levels of galanin (20.2 pg/mL versus 26.4 pg/mL, p = 0.002) and higher concentrations of glypican-4 (3.1 ng/mL versus 2.6 ng/mL, p < 0.001) than controls. Both adipokines were correlated positively with body mass index (BMI), insulin, triglyceride and Homeostasis Model Assessment (HOMA) index; glypican-4 also showed positive correlations with fasting blood glucose, free testosterone, modified Ferriman-Gallwey scores (p < 0.05). Multiple Linear Regression analyses showed that PCOS and BMI were the best predictors affecting galanin levels with a decreasing and increasing effect respectively; however BMI was the best predictor affecting glypican-4 levels with an increasing effect (p < 0.001). Conclusion: Galanin levels were lower and glypican-4 levels were higher in women with PCOS than controls. Further studies are needed to determine whether these adipokines could be used as additional markers for insulin sensitivity and lipid profile and whether they might play a role in the pathogenesis of PCOS, in which metabolic cardiovascular risks are increased.
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Humans , Female , Polycystic Ovary Syndrome/complications , Insulin Resistance , Galanin/blood , Glypicans/blood , Heart Disease Risk Factors , Cardiovascular Diseases/etiology , Body Mass Index , Case-Control Studies , Risk FactorsABSTRACT
Objective To explore the expression and function of galanin and its receptor in the female mice of anxiety-and depression-like behavior.Methods In situ hybridization was used to detect the expression of galanin,GalR1,GalR2 and GalR3 in the hippocampus of C57BL/6J female mice.A total of thirty female mice was divided into two groups:experiment group (n=15) and control group (n=15).The experiment group was subjected to the chronic unpredictable mild stress (CUMS) for four weeks,and the control group was not subjected to any treatment.Four weeks later,a series of tests were performed on those two groups,including the sucrose preference test,the novel object recognition test,the open field test and suspension tail test.After behavior tests,the hippocampus RNA was extracted from eight mice in each group to test the expression of galanin and its receptor through qPCR.The rest part of mice were used to mark C-Fos immunostaining in the dentate gyms (DG) of hippocampus.Results The result of in situ hybridization showed that galanin,GalR1 and GalR2 distributed in the Hillus of ventral hippocamous,GalR3 had no positive signal.In the sucrose preference test,the experiment group drunk less sucrose when compared with the control group (P＜0.05).In the novel object recognition test,the experiment group contacted shorter time to the novel object when compared with the control group (P＜0.05).In the open field test,the experiment group had shorter in session time when compared with the control group (P＜0.05).In the suspension tail test,the experiment group had longer immobility time when compared with the control group (P＜0.05).The qPCR result showed that the higher expression of galanin and GalR1 in the hippocampus of experiment group (P＜0.05).More C-Fos positive cells in the DG of hippocampus of experiment mice were immunostained (P＜0.05).Conclusions Galanin,GalR1 and GalR2 mainly distribute in the Hillus of the ventral hippocampus.Galanin may be involved in the anxiety-and depression-like behavior of C57BL/6J through GalR1.
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Objective To explore the effect of galanin ( GAL) on locus coeruleus ( LC) neurons from neonatal rat and mechanism with its receptor GalR and potassium channel.Methods Brain slices from neonatal rats were prepared and the resting membrane potential and spontaneous action potential of LC neurons were recorded with whole cell patch-clamp configuration.GAL, AR-M1896 and potassium channel blockers were bath applied with different concentration.Results Bath application GAL induced hyperpolarization and inhibited firing rate of LC neurons.However, AR-M1896 ( a selective GalR2 agonist) did not induce significant effect on LC neurons, only at very high concentration(1μM) it induced slight hyperpolarization and reduced firing rate.The inhibitory effect of GAL was partially blocked by TEA ( an antagonist of voltage-dependent potassium channel) and significantly blocked by BaCl2(an antagonist of inward-rectifying potassium channels), while other potassium channels blockers such as Glybenclamide(ATP-sensitive potassium channel blocker),Charybdotoxin(large-conductance Ca2 +-activated K + channels blocker),Apamin(small-conductance Ca2 +-activated K +channels blocker) failed to block it.Conclusion GAL inhibits LC neurons from neonatal rats, mainly through GalR1.TEA-sensitive potassium channels and inward-rectifying potassium channels, but not ATP-sensitive potassium channel and calcium-activated potassium channel, are involved in this inhibition.
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Objective To explore the effect of intracerebroventricular injection of AR-M1896, a galanin receptor 2 agonist, on depres-sion-like behavior in rat chronic mild stress (CMS) model. Methods 48 Sprague-Dawley rats were randomly assigned into control group, CMS group, CMS artificial cerebrospinal fluid (aCSF) group and CMS AR-M1896 group equally. The control group received no interven-tion, and the other groups were established chronic mild stress model. After six-week of stress, forced swim test and sucrose preference test were conducted to identify the CMS rats. AR-M1896 or aCSF was injected into the lateral ventricle of CMS AR-M1896 group and CMS aC-SF group, respectively. The immobility time and climbing time in the forced swim test were analysed, and the sucrose consumption percent-age in the sucrose preference test was measured. Results The immobility time decreased (F=11.998, P<0.01), climbing time increased (F=8.268, P<0.05), and the sucrose consumption percentage increased (F=10.352, P<0.01) in CMS AR-M1896 group, compared with CMS aC-SF group. Conclusion Intracerebroventricular administration of galanin receptor 2 agonist AR-M1896 is effective on depression in CMS model rats.
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Stroke leads to a variety of pathophysiological conditions such as ischemic infarct, cerebral inflammation, neuronal damage, cognitive decline, and depression. Many endeavors have been tried to find the therapeutic solutions to attenuate severe neuropathogenesis after stroke. Several studies have reported that a decrease in the neuropeptide regulator ‘galanin’ is associated with neuronal loss, learning and memory dysfunctions, and depression following a stroke. The present review summarized recent evidences on the function and the therapeutic potential of galanin in post-ischemic stroke to provide a further understanding of galanin's role. Hence, we suggest that galanin needs to be considered as a therapeutic factor in the alleviation of post-stroke pathologies.
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Depression , Galanin , Inflammation , Learning , Memory , Neurons , Neuropeptides , Pathology , StrokeABSTRACT
Objective To study the expression and role of galanin in the hypothalamus of rat with the drug-induced hyperprolactinemia.Methods Hyperprolactinemia was induced by daily intraperitoneal injections 50 mg/kg sulpiride solution.The protein in the hypothalamus of rat was extracted to determine the expression levels of galanin with Western Blot.The expression and colocalization of galanin and dopamine in model and control group were observed with immunofluorescence.Results The model group showed a significant increase of serum prolactin (PRL) level and a significant decrease of serum estradiol (E2) level,as compared to the control group ((15.74±2.49) ng/ml vs (10.25±1.29) ng/ml and (4.24±0.69)pg/ml vs (9.56±3.25) pg/ml,respectively,P＜0.05).Both the expression level of galanin and the number of neurons coexisting with galanin and dopamine were decreased in the hypothalamus of the hyperprolactinemia rat compared with the control group.Western Blot revealed that,compared to the control group,the sulpiride model group had a significant increase of galanin but not TH (0.405±0.112 vs 0.985±0.158,P＜0.05 and 0.871 ± 0.046 vs 0.890±0.054,P＞ 0.05,respectively).Conclusion Galanin expression level has decrease in the hypothalamus of the hyperprolactinemia rat,which contributes to the reduction of dopaminergic neurons.
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Background:Gastric ischemia-reperfusion injury often leads to calcium overload,excessive free radical production, leukocyte infiltration and microcirculation disturbance.Post hypoxic treatment can effectively reduce the injury induced by hypoxia/reoxygenation (H/R).Galanin receptor 2 (GalR2)is distributed mainly in the digestive and nervous system, which can regulate many endocrine activity.However,the protective effect of GalR2 on human gastric epithelial cells injury induced by H/R is not clarified.Aims:To investigate the protective effect and its mechanism of GalR2 agonist post-conditioning on human gastric epithelial cells injury induced by H/R.Methods:H/R model was constructed on human gastric epithelial cells GES-1.Normal control group (N group),H/R group,M1145 (GalR2 agonist)treatment group (M group),SB203580 (p38MAPK inhibitor) +M1145 treatment group (S +Mgroup)and DMSO solvent control group (D group)were established.Survival rate of cells was measured by MTT assay.Apoptosis rate of cells was determined by flow cytometry,and cell apoptosis was examined by Hoechst staining.Level of lactate dehydrogenase (LDH)was measured by ELISA.Expressions of Bcl-2,Bax and p38MAPK were determined by real-time quantitative PCR.Results:Survival rate of cells was significantly lower in H/R group than that in N and M groups (P <0.05 ).Apoptosis rate of cells was significantly higher in H/R group than that in N,M and S +M groups (P <0.05 ),and apoptosis rate of cells was significantly lower in Mgroup than that in S +M group (P <0.05).Expression of LDH was significantly higher in H/R group than that in Mand S +Mgroups (P <0.05).Expression of Bcl-2 was significantly higher in N and M groups than that in H/R,S +Mand D groups (P <0.05);expression of Bax was significantly higher in H/R group than that in N,M and S +Mgroups (P <0.05);expression of p38MAPK was significantly lower in H/R and S +M groups than that in M group (P <0.05 ).Conclusions:GalR2 agonist M1145 plays an effective role in reducing the injury of GES-1 cells induced by H/R,the effect may be conducted through p38MAPK pathway.
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Galanin is a peptide with wide-ranging effects,especially within the central,peripheral nervous system and endocrine system.Many tumors of neuroendocrine origin,and also an increasing number of non-neuroendocrine cancers,have been shown to express galanin and/or its receptors.Expression of galanin peptide has been detected in pheochromocytoma,squamous cell carcinoma,pituitary adenoma,gastrointestinal cancers and so on.Galanin peptide plays an important role in tumori-genesis and progression of many kinds of tumors.Therefore,studying the roles of galanin and its receptors are helpful for diagnosis and treatment of tumors.
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Objective To study the protective effect of galanin on 2,3-Dimethoxy-1,4-naphthoquinone (DMNQ)-induced oxidative stress and cell damage in HEK-293A cells and its possible mechanisms.Methods The expression of galanin and its three receptors (GalR1-3) in HEK-293A were determined with RTPCR technique.The cultured HEK-293A cells were divided into four groups:Control,DMNQ,DMNQ + GAL and DMNQ + AR-M1896 and the cell viability was measured with CellTiter 96 AQueous One Solution Cell Proliferation Assay (MTS).Results The RT-PCR data revealed the presence of galanin and its receptors in HEK-293A cells.The expression level was in the order of GalR2 =Galanin ＞ GalR3 ＞ GalR1.DMNQ caused oxidative stress and cell damage in HEK-293A cells with a dose-dependent manner with an IC50 =13.4 μM.Application of galanin reduced the DMNQ-induced cellular toxicity in HEK-293A,which increased cell viability by 24.4％ and 18.8％ in 1 μM and 100 nM,respectively.AR-M1896,an agonist of GalR2 had a similar effect,increased cell viability by 8.7％ and 8.9％ in 1 μM and 100 nM,respectively.Conclusion These data suggest that galanin has a protective effect on DMNQ-induced oxidative stress and cell damage in HEK-293A cells,probably mediated by GalR2.
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Objective To study the expression and significance of galanin (GLA) in the prostate carcinoma (PCa).Methods The samples from 50 patients with benign prostatic hyperplasia (BPH) and 50 patients with PCa and 30 PCa patients with bone metastasis were examined by immunohistochemical staining.Results The positive rates of GLA expression in BPH,PCa,and PCa with bone metastasis were 18 ％ (9/50),68 ％ (34/50),and 80 ％ (24/30),respectively,and there were statistically significant differences between PCa patients,PCa patients with bone metastasis and BPH patients (x2 =25.5,29.74,both P ＜ 0.01),but there was no significant difference between PCa patients and PCa patients with bone metastasis (x2 =1.35,P ＞ 0.05).Conclusion GLA has higher expression in prostatic cancer cells,it might be an important indicators for differentiating prostate cancer from benign prostatic hyperplasia and predicting the prognosis of prostate carcinoma.
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The present study examines the role of cerebroventricular administered (IIIrd ventricle) galanin on LHRH and LH release in adult and immature male rats. In both age groups, galanin stimulated LHRH synthesis and release from the hypothalamus, leading to a higher release of pituitary LH which in turn increased plasma LH levels. Galantide, a galanin receptor blocker, on the other hand, drastically reduced hypothalamic LHRH and plasma LH while increasing pituitary LH. In vitro incubation of anterior pituitary cells with galanin followed by LHRH resulted in increased release of pituitary LH but not by galanin alone. Galantide exhibited no such effect either alone or with LHRH. These results indicate that galanin is an important regulator for both hypothalamic LHRH and hypophysial LH and its role is independent of age in the case of male rats.
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Aim To observe the effects of galanin (Gal) antagonist M35 or M40 at different concentrations on the Gal evoked outward current in principal trigeminal nucleus (PrV) neurons. Methods The technique of whole cell patch clamp was used to record the change of membrane current. Results At doses of M35 0.01 , 0.03 and 0.1 ?mol?L -1 , the Gal evoked outward current decreased by 53.1 %, 40.4 % and 27.2 %,respectively. While M35 1 and 3 ?mol?L -1 , the current increased by 16.2 % and 38.4 %. At doses of M40 0.01 and 0.03 ?mol?L -1 ,the current increased by 93.7 % and 68.4 %,while for M40 0.3 ,1 and 3??mol?L -1 , the current decreased by 49.2 %, 69.9 % and 87.2 %, respectively. Conclusion M35 at low concentrations antagonizes the effect of Gal and at high concentrations acts as a Gal receptor agonist. Whereas M40 in high doses antagonizes the effect of Gal and in low doses exerts an autagonistic action. There may be different Gal subtype receptors in the same PrV neuron.
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Within the medial preoptic area[MPOA], several cytoarchitectonically defined cell groups are sexually dimorphic in their morphology. Specially, the sexual dimorphic nucleus of the preoptic area[SDN-POA] is reported an example of a morphological sex difference in the rat hypothalamus which is influenced by gonadal steroid hormones. Thus, we detemined the distribution of Galanin-immunoreactive[Gal-I] cells and fibers within MPOA and their morphological response to gonadal steroids which is influenced by gonadectomy or prenatal restosterone treatments were observed. The Gal-I cells were appeared within the medial preoptic area. In the males, the volume and number of Gal-I nerve cell bodies were greater than that of females. But the female which treated prenatal testosterone injection had many Gal-I neurons than infact female. And the males that decreased the volume of gonadal hormone by gonadectomy were decreased the volume and number of Gal-I neurons than that of normal males. These results suggest that galaninergic cells within the medial preoptic area are influenced by gonadal steroid hormone[testosterone] in the regulation of sexually dimorphic function.
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Animals , Female , Humans , Male , Rats , Galanin , Gonadal Steroid Hormones , Gonads , Hypothalamus , Immunohistochemistry , Neurons , Preoptic Area , Sex Characteristics , Steroids , TestosteroneABSTRACT
The characteristics of distribution, origin and properties of galanin (GAL) were investigated, by using immunocytochemistry (the whole mount stretched pr- eparations and cryostat sections), immunoelectronmicroscopy and microspectroph- ometer measuring techniques. The results showed that (1) All layers of small intestine were rich in GAL- immunoreactive(GAL-I) nerves with a high density in myenteric and submucosal plexuses. (2) A rather high density around the small blood vessels of the small intestine and intestinal crypts were observed. Some GAL-I neurons were seen in the myenteric and submucosal plexuses. Enteric GAL-I nerve fibers seemed to be endogenic and probably related to the regulation of motor function in the gastro- intestinal tract, since there was no obvious reducation of nerve fibers after sec- tion of mesenterium or injection of capsaicin. (3) The distribution and charac- teristics of GAL-I nerve fibers in small intestine indicated that the GAL-I ne- rves might be playing a regulational role in the motion, absorption, secretion and regional blood flow of the gastrointestinal tract.
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Objective:To elucidate the possible role of galanin in the development of experimental depression in rats. Methods:Openfield was performed to test the behavior of rats. The changes of the galanin level in different brain areas were determined by RIA. The effect of fluoxetine hydrochloride on galanin level were observed by intraperitoneal injection. Results:Compared to control group, the crossing times and rearing times decreased significantly in depressed rats, galanin level decreased remarkably in plasma, hypothalamus, hippocampus, forebrain, parietal lobe and temporal cortex of depressed rats. Intraperitoneal injection of fluoxetine hydrochloride obviously improved the depressed behavior in rats, increased the galanin level in the hippocampus and forebrain of depressed rats. Conclusion:Hippocampus and forebrain may be involved in the development of experimental depression and in the antidepressive effects of fluoxetine hydrochloride.
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changes of galanin in the small intestines of the rats which were inflicted with acute intestinal radiation sickness (AIRS) by exposing to 20 Gy gamma rays were studied with immunocytochemistry (ICC) , HE staining of tissue sections, and microspectrophotometer. It was found that the damage of intestinal mucosa was being intensified as AIRS progressed; there no marked change of GAL-LI neurons but the arrangement of GAL-LI fibers was disordered in the irradiated rats as compared with those of the control; the galanin content of the small intestines was significantly tower in the irradiated rats than in the control especially in the 48th and 72nd hour after irradiation (P
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Comparative investigation of the distribution of galanin-immunoreactive (GAL-ir) nerve fibers in the neural lobe of the human being, monkey, dog, cat and rat was studied immunohistochemically. The density of GAL-ir fibers in the posterior pituitary was highest in the dog and rat, moderate in the monkey and cat; and lowest in the human being. A dense accumulation of positive fibers appeared in the pituitary stalk bordoring the intermediate lobe. The fiber density in the central part of the posterior pituitary was slightly higher than at its periphery in the human and monkey. Moderate amount of fibers were found to spread all over the neural lobe of the dog and rat, with slightly higher density in the posterior part of the dog. In the cat, the highest density of GAL-ir fibers was found along the wall of the recess hypophysis. A slightly increasing fibers or fiber clumps were seen in the peripheral region of posterior pituitary in four species of the animals and human being. Some fibers were found surrounding the blood vessels or located in their walls.
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Aging changes of neurotensin-like (NT-L) and galanin-like (GAL-L) cell bodies and fiber terminals in the central amygdaloid nucleus between the young and old rats were studied by means of immunohistochemical and microspectrophotometric techniques. NT-L cell bodies were mainly located in the central part (CeLn) of, centrolateral amygdaloid nucleus, a few of NT-L neurons were also found in the centrolateral amygdaloid nucleus, capsular part (CeLc) and centromedial amygdaloid nucleus (CeM). NT-L fiber terminals were seen mainly in the CeLn and CeLc. GAL-L cell bodies were observed only in the CeM. A marked decrease of density of NT-L cell bodies and fiber terminals in the central amygdaloid nucleus was found in the old rats as compared with young animals. No significant age difference in number of GAL-L cell bodies was observed in the central amygdaloid nucleus, but the staining intensity of GAL-L cell bodies was reduced remarkably. The results show that there are apparent changes with aging of the NT-L and GAL-L neurons in the central amygdaloid nucleus of the rat. The significance of the changes remains to be studied further.