WDR5 promotes the tumorigenesis of oral squamous cell carcinoma via CARM1/ß-catenin axis.

Oral squamous cell carcinoma (OSCC) is a malignancy all over the world. WD repeat domain 5 (WDR5) is involved in cancer progression. In addition, it was reported that WDR5 is upregulated in head and neck cancer, while its role in OSCC is unknown. First, the expression of WDR5 in oral cancer tissues and cells was examined by qRT-PCR, IHF and western blot. CCK-8 assay was performed to test the cell viability. Cell migration was assessed by transwell assay. Knocking down WDR5 or CARM1 in oral cancer cells to detect its function on cancer growth, WDR5 and CARM1 were significantly upregulated in OSCC. Silencing WDR5 suppressed OSCC cell viability and migration. CARM1 level in OSCC cells was significantly inhibited by WDR5 downregulation, and CARM1 elevation could rescue the effect of WDR5 knockdown on tumorigenesis of OSCC. Moreover, silencing of WDR5 notably inactivated ß-catenin signaling pathway, while this phenomenon was restored by CARM1 overexpression. Silencing of WDR5 attenuated the tumorigenesis of OSCC via CARM1/ß-catenin axis. Thus, WDR5 might be a target for OSCC treatment.

The variation in the levels of 18 amino acids in the cortex and plasma of cerebral ischemia C57BL/6 mice.

Emerging evidence suggests that amino acid (AA) neurotransmitters play important roles in the pathophysiological processes of cerebral ischemia. In this work, an HPLC with fluorescence detection (HPLC-FLR) method was developed for the simultaneous determination of 18 AAs in the cortex and plasma after cerebral ischemia in mice. The ischemia model was prepared by bilateral common carotid artery occlusion, and then the cortex and plasma of the sham, ischemia, and naringenin groups were collected. Based on the protein precipitation method, a simple and effective sample preparation method was developed. The treated sample contained minimal proteins and lipids. The analysis of the sample was performed by the proposed HPLC-FLR method in combination with o-phthalaldehyde. The results showed a statistically significant increase in excitatory AAs (aspartic acid and glutamic acid), inhibitory AAs (glycine and 4-aminobutyric acid), phenylalanine, citrulline, isoleucine, and leucine levels, and a decrease of glutathione and phenylalanine levels when compared with the sham group in the cortex. Besides, the administration of naringenin had significant effects on excitatory AAs, inhibitory AA (glycine), glutamine, tyrosine, phenylalanine, and leucine levels when compared with the sham group in the cortex. These findings could be utilized in studying and clarifying the mechanisms of ischemia.

Long-term hygroscopic dimensional changes of core buildup materials in deionized water and artificial saliva.

The dimensional stability of core buildup materials plays an important role in clinical application. In this study, hygroscopic dimensional changes of four commercial core buildup materials were investigated in deionized water and artificial saliva for up to 150 days. Specimens were made within a customized cylindrical mold. The initial mass and the apparent mass in liquids were measured. All the tested materials showed hygroscopic expansion after a 150-days immersion time. Hygroscopic expansion of these four materials can partly compensate for the polymerization shrinkage. SDR showed the lowest hygroscopic expansion of the four tested materials when immersed in deionized water and artificial saliva. PC showed the highest hygroscopic expansion in deionized water, while LC showed the highest hygroscopic expansion in artificial saliva. In the case of different immersion solvents, osmotic pressure should be considered. For hygroscopic dimensional changes, the hydrophilicity of monomers and changes of intermolecular forces may be crucial factors.

Antidepressant mechanisms of venlafaxine involving increasing histone acetylation and modulating tyrosine hydroxylase and tryptophan hydroxylase expression in hippocampus of depressive rats.

Venlafaxine (VEN) is a widely used antidepressant as a serotonin-reuptake and norepinephrine-reuptake inhibitor. It is used primarily in depression, especially with generalized anxiety disorder or chronic pain. This medicine is of interest because its mechanisms involved multiple aspects. In the current study, the antidepressant action of VEN was investigated by studying the histone acetylation and expression of tyrosine hydroxylase (TH) and tryptophan hydroxylase (TPH) in rats exposed to chronic unpredicted stress (CUS) for 28 days. Male Sprague-Dawley rats were divided into a control group, VEN-treated control group, CUS group, and VEN-treated CUS group. VEN (23.4 mg/kg once daily) was administered to rats by intragastric gavage, whereas the same volume of vehicle was given to rats in the control and model groups. Rat behaviors, acetylated H3 at lysine 9 (acH3K9), acetylated H3 at lysine 14 (acH3K14), acetylated H4 at lysine 12 (acH4K12), histone deacetylase 5, and TH and TPH expression in the hippocampus were determined. Chronic VEN treatment significantly relieved the anxiety- and depression-like behaviors, prevented the increase of histone deacetylase 5 expression and decrease of acH3K9 level, and promoted TH and TPH protein expression in the hippocampus of CUS rats. The results suggest that the preventive antidepressant mechanism of VEN is partly involved in the blocking effects on histone de-acetylated modification and then increasing TH, TPH expression.

[Gastrodin improves hippocampal neurogenesis by NO-cGMP-PKG signaling pathway in cerebral ischemic mice].

This paper was aimed to investigate the effect of gastrodin( GAS) on hippocampal neurogenesis after cerebral was chemic and to explore its mechanism of action related to NO. The cerebral ischemia model of C57 BL/6 mice was established by bilateral common carotid artery occlusion. The pathological changes in hippocampal CA1 region and the cognitive function of mice were assessed by HE staining and Morris water maze test,respectively. The count of Brd U/Neu N positive cells in dentate gyrus was detected by immunofluorescence assay. The NOS activity and the NO content were determined by colorimetric and nitrate reduction methods,respectively.The level of c GMP was measured by ELISA kit,and the PKG protein expression was tested by Western blot. On postoperative day 8,the hippocampal CA1 pyramidal neurons of mice showed irregular structure,with obvious nuclear pyknosis,loose cell arrangement and obvious decrease in the number of neurons. On postoperative day 29,the spatial learning ability and memory were decreased. These results indicated cerebral ischemia in mice. Meanwhile,the Brd U/Neu N positive cells were increased significantly in ischemic mice,indicating that neurogenesis occurred in hippocampus after cerebral ischemia. Treatment with different doses of gastrodin( 50 and 100 mg·kg-1) significantly ameliorated the pathological damages in the CA1 region,improved the ability of learning and memory,and promoted hippocampal neurogenesis. At the same time,both the NOS activity and the NO concentration were decreased in model group,but the c GMP level was increased,and the PKG protein expression was up-regulated. Gastrodin administration activated the NOS activity,promoted NO production,further increased c GMP level and up-regulated PKG protein expression. These results suggested that gastrodin can promote hippocampal neurogenesis after cerebral ischemia and improve cognitive function in mice,which may be related to the activation of NO-cGMP-PKG signaling pathway.

Simultaneous determination of nine analytes related to the pathogenesis of diabetic encephalopathy in diabetic rat cortex and hippocampus by HPLC-FLD.

The determination of amino acids and monoamine with actions like neurotransmitters or modulators has become increasingly important for studying the relationship between the dysfunction of neurotransmitters and the pathogenesis of diabetic encephalopathy. Here, a high-performance liquid chromatography with fluorescence detection method was developed to simultaneously determine nine monoamines and amino acids including three excitatory neurotransmitters (aspartate, glutamate, and serotonin), four inhibitory neurotransmitters (glycine, γ-aminobutyric acid, taurine, dopamine), a precursor of 5-HT (tryptophan) and methionine using homoserine as the internal standard. The separation was performed on a BDS column with methanol-buffer solution of 35 mmol/L sodium acetate and 5 mmol/L citric acid (pH 6.0) using a simple gradient elution. Several parameters including specificity, precision, and recovery were validated after optimization of the analytical conditions. The developed method was successfully applied to determine the cortex and the hippocampus samples from Sprague-Dawley rats. Our results showed that various neurotransmitters involved in diabetes mellitus may tend to be differentially modulated and present a different alteration tendency at different time course, which might be associated with the duration of diabetes mellitus.

Abnormal modification of histone acetylation involved in depression-like behaviors of rats induced by chronically unpredicted stress.

Depression is a complex multifactorial mental disorder. Its etiology involves many factors such as social environments, genetics, and psychology. Recent studies have shown that epigenetic modification may be associated with depression. Histone acetylation is one of the main mechanisms of epigenetic modification and plays an important role in genetic expression. In this study, we investigated the role of histone acetylation in the depression-like behaviors of rats undergoing chronically unpredicted stress (CUS) by detecting the mRNA and protein expression of histone deacetylase 5, cAMP-response element-binding protein, and the level of histone acetylated modification of H3K14, H3K23, and H4K16 in the prefrontal cortex and hippocampus of the rats. The results showed that significantly increasing depression-like behaviors were observed with a decreasing histone acetylated modification level, especially on acytelated-H3K14, acytelated-H3K23, and acytelated-H4K16, upregulating histone deacetylase 5 expression and downregulating cAMP-response element-binding protein expression in CUS rats, compared with control rats. The results indicate that the decrease in the histone acetylation modification level may be partly involved in the mechanism of depression-like behaviors of rats induced by CUS.

Infliximab ameliorating depression-like behavior through inhibiting the activation of the IDO-HAAO pathway mediated by tumor necrosis factor-α in a rat model.

In recent years, some studies have suggested that the activation of inflammatory system plays a role in the occurrence of depression. Tumor necrosis factor-α (TNF-α), as one of the preinflammatory cytokines, has been reported to be involved in the occurrence of various diseases including depression. Infliximab, an antagonist of TNF-α, is usually used to treat some autoimmune diseases such as Crohn's disease and can perhaps be used to treat other diseases. In this study, the antidepressant effect and a possible mechanism of infliximab were investigated by studying the depression-like behavior and expression of TNF-α, indoleamine 2, 3-dioxygenase (IDO), and 3-hydroxyl amino acid oxygenase (HAAO) from the cortex and hippocampus in rat exposed to chronic unpredicted stress. Forty male Sprague-Dawley rats were divided into a control group (CG), an infliximab-treated control group, a model group (MG), and an infliximab-treated model group (IFXM). Infliximab (5 mg/kg once week) was administered to the infliximab-treated control group and IFXM rats by an intraperitoneal injection, whereas an equivalent volume of vehicle was administered to CG and MG rats. Rat behaviors and the expression of TNF-α, IDO, and HAAO in the cortex and hippocampus were determined. It was found that a significant relief in depression-like behaviors was observed with a downregulation of TNF-α, IDO, and HAAO expression in the IFXM rats compared with MG rats. The results show the antidepressant effect of infliximab and suggest that its mechanism is partly related to inhibition of IDO-HAAO pathway activation mediated by TNF-α in rat brain.

[Effect and mechanism of polydatin on diabetic myocardial hypertrophy in mice].

To observe the preventive effect of polydatin on diabetic myocardial hypertrophy in mice and discuss its and mechanism. The diabetic model was induced with low dose STZ (40 mg x kg(-1) x d(-1) x 5 d, ip) for five days in mice. The myocardial hypertrophy was determined by hypertrophy indexes (LVHI, left ventricular/right ventricle and septum), left ventricular/body weight (LV/BW), the histological examination and the mRNA expression of atrial natriuretic factor(ANF). The fast blood glucose(FBG), serum insulin and plasma hemoglobin A1c ( HbA1c) levels were detected, and then HOMA insulin resistance index ( HOMA. IR) was calculated. The mRNA and protein expressions were measured by qRT-PCR and western blotting, respectively. According to the results, the FBG of the model group exceeded 11.1 mmol x L(-1), with notable decrease in BW and significant increase in insulin, HbA1c and HOME. IR, suggesting the successful establishment and stability of the diabetic model. The increases in LVHI, LV/BW, cell surface and ANF mRNA indicated a myocardial hypertrophy in diabetic mice. Meanwhile, the model group showed decrease in mRNA and protein expressions of PPARß and significant increase in NF-κB p65, COX-2 and iNOS expressions. After the preventation with PD (50, 100 mg x kg(-1) x d(-1)), diabetic mice showed increase in BW, reduction in the levels of FBG, insulin and HbA1 c, relief in insulin resistance and significant recovery in hypertrophy indexes, indicating PD has the protective effect in diabetic myocardial hypertrophy. Meanwhile, PD up-regulated the expression of PPARß, inhibited the expressions of NF-κB p65, COX-2 and iNOS, demonstrating that PD's protective effect may be related to the activation of PPARß and the inhibition of NF-κB, COX-2 and iNOS signaling pathways.

[A brief talk on the embodiment of Three-Layer thought in the science of acupuncture and moxibustion].

Three-Layer thought is an important proposition in Chinese traditional philosophy. This thought embodies the Chinese people's cosmology and methodology and exerts a far-reaching influence on various aspects of Chinese culture. The embodiment of Three-Layer thought in the theory and practice of acupuncture and moxibustion from naming of acupoints, principles of treatment, needling instruments, prescription of acupoints as well as needling techniques is elaborated and briefly analyzed. Thus it illustrates the comprehensive application of Three-Layer thought in acupuncture and moxibustion through the history and the significance of Chinese traditional philosophy in the science of acupuncture and moxibustion.

[Baicalin suppresses beta-amyloid protein induced hippocampal cyclooxygenase-2 expression].

OBJECTIVE: To study the brain protection of baicalin on rats with Alzheimer's disease (AD) and its probable mechanism of action. METHODS: Thirty-six male healthy Wistar rats were randomly divided into the sham-operative group, the AD group, and the baicalin group, twelve in each. beta-amyloid protein 1-40 was injected to the bilateral hippocampus of rats in the AD group and the baicalin group to establish the AD rat model. The sham operation was performed to rats of the sham-operative group in the same way. Equal volume of 0.9% sodium chloride solution was injected to the bilateral hippocampus of rats in the sham-operative group. Baicalin was intraperitoneally injected at the daily dose of 40 mg/kg to rats in the baicalin group before and after operation, once daily for 7 successive days. Equal volume of buffer solution was intraperitoneally injected to rats in the sham-operative group and the AD group in the same procedures at the same time points. The expression of hippocampal cyclooxygenase-2 (COX-2) was determined by Western blot. The spatial learning memory capacities was observed using T-morris test. Histological changes were observed using hematoxylin-eosin (HE) staining. RESULTS: Results of the T-morris test showed the spontaneous alternation selective ratio decreased in the AD group (28.33% +/- 7.50%) and the baicalin group (38.33% +/- 7.50%) (both P < 0.05) when compared with the sham-operative group (61.67% +/- 7.50%). There was significant difference between the AD group and the baicalin group (P < 0.05). Results of HE staining showed degeneration and necrosis of cortical and hippocampal neurons in the AD group and the baicalin group. Changes in the AD group were more obvious. Results of Western blot showed the expression of hippocampal cyclooxygenase (COX-2) obviously increased in the AD group, while it obviously decreased in the baicalin group (P < 0.05). CONCLUSION: Baicalin could alleviate beta-amyloid protein induced brain injury, which might be associated with its inhibition on the COX-2 expression.

Reduced brain-derived neurotrophic factor expression in cortex and hippocampus involved in the learning and memory deficit in molarless SAMP8 mice.

BACKGROUND: The molarless condition has been reported to compromise learning and memory functions. However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to find the molecular mechanism related with learning and memory deficit after a bilateral molarless condition having been surgically induced in senescence-accelerated mice/prone 8 (SAMP8) mice, which may ultimately provide an experimental basis for clinical prevention of senile dementia. METHODS: Mice were either sham-operated or subjected to complete molar removal. The animals' body weights were monitored every day. Learning ability and memory were measured in a water maze test at the end of the 1st, 2nd, and 3rd months after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, the locomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex and hippocampus were dissected for Western blotting to measure the expression levels of brain-derived neurotrophic factor (BDNF) and the tropomyosin related kinase B (TrkB), the high affinity receptor of BDNF. RESULTS: Slightly lower weights were consistently observed in the molarless group, but there was no significant difference in weights between the two groups (P > 0.05). Compared with the sham group, the molarless group exhibited lengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activity was observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarless group (P < 0.05); but the expression of its receptor, TrkB, was not significantly affected. CONCLUSION: These results suggested that the molarless condition impaired learning and memory abilities in SAMP8 mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression in the cortex and hippocampus.

[The support of National Natural Science Foundation of China prompts the progress and development of basic research of dental and craniofacial research: a 25 years review].

OBJECTIVE: To investigate the effect of National Natural Science Foundation of China (NSFC) on the progress of dental research from 1986 to 2010. METHODS: The data regarding the NSFC allocated to dental and craniofacial research from 1986 to 2010 were collected. Total expenses and numbers of the majority of programs and the situation of completed program finished in recent 7 years were provided. RESULTS: From 1986 to 2010, a total of 922 projects and 204 401 thousands Chinese Yuan supported by NSFC were allocated to dental research. The detailed allocations were as follows: general program (564), young scientists fund (258), regional fund (40), key program (11), national science fund for distinguished young scholars (5), major international (regional) joint research program (1), others (43). The grants of talent training increased dramatically. Taking the projects (307) completed between 2003 and 2009 for example, 307 papers were published in Science Citation Index (SCI) included journals and 1049 papers were published on Chinese journals. By the time of completion of the projects, 39 post-doctoral students, 590 students for PhD degree and 670 students for Master degree had been trained. CONCLUSIONS: Over the past 25 years, the continuous increase of NSF on dental research has led to substantial achievement, resulting in great progress of dental oral-cranio-facial research.

Inhibitory effect of ginsenoside Rb1 on calcineurin signal pathway in cardiomyocyte hypertrophy induced by prostaglandin F2alpha.

AIM: To examine the antihypertrophic effect of ginsenoside Rb1 (Rb1) induced by prostaglandin F2alpha(PGF2alpha) in vitro and to investigate the possible mechanisms involved in the calcineurin (CaN) signal transduction pathway. METHODS: The cardiomyocyte hypertrophy induced by PGF2alpha and the antihypertrophic effect of Rb1 were evaluated in primary culture by measuring the cell diameter, protein content, and atrial natriuretic peptide (ANP) mRNA expression. ANP and CaN mRNA expressions, CaN and its downstream effectors NFAT3 and GATA4 protein expressions, and the intracellular free Ca2+ concentration ([Ca2+]i) were assayed by RT-PCR, Western blot, and fluorescent determination using Fura 2/AM, respectively. RESULTS: PGF2alpha (100 nmol/L) significantly increased the cardiomyocyte diameter, protein content and [Ca2+]i, and promoted ANP, CaN mRNA, and CaN/NFAT3/GATA4 protein expressions, which were inhibited by either Rb1 in a concentration-dependent manner (50, 100, and 200 microg/mL) or L-arginine (1 mmol/L). NG-nitro-L-arginine-methyl ester, a nitric oxide synthase inhibitor, could abolish the effects of L-arginine, but failed to change the effects of Rb1 in the experiments above. CONCLUSION: The present data implicate that Rb1 attenuates cardiac hypertrophy, the underlying mechanism may be involved in the inhibition of the Ca2+-CaN signal transduction pathway.

Inhibitory effect of ginsenoside Rb1 on cardiac hypertrophy induced by monocrotaline in rat.

Ginseng, the root of Panax ginseng, has been used as folk medicine in the treatment of various diseases for thousands of years in China. Ginsenoside Rb1 (Rb1), one of the effective components of ginseng, has been reported to release nitric oxide and decrease intracellular free Ca2+ in cardiac myocytes, both of which play important roles in antihypertrophic effect. This study was to investigate the potential effect of Rb1 on right ventricular hypertrophy (RVH) induced by monocrotaline (MCT) and its possible influence on calcineurin (CaN) signal trasnsduction pathway. MCT-treated animals were administered with Rb1 (10 and 40 mg /kg) from day 1 to day 14 (preventive administration) or from day 15 to day 28 (therapeutic administration), or with vehicle as corresponding controls. After 2 weeks, significantly hypertrophic reactions, including RVH index and the expressions of atrial natriuretic peptide mRNA, appeared in right ventricle of all MCT-treated animals (p < 0.05), which were significantly decreased with some improvements of myocardial pathomorphology in both Rb1 prevention- and therapy-groups (p < 0.05). Similarly, MCT-treatment caused the high expressions of mRNA and/or proteins of CaN, NFAT3 and GATA4 from cardiocytes (p < 0.05) and Rb1 could alleviate the expressions of these factors above (p < 0.05). These results suggest that Rb1 treatment can inhibit the RVH induced by MCT, which may be involved in its inhibitory effects on CaN signal transduction pathway.

[Brief discusion on importance of accurate location in acupuncture treatment for periarthritis of shoulder].

Briefly discuss some recognation problems about acupuncture treatment of periarthritis of shoulder at present and put forward the methods for diagnosis and acupuncture treatment based on accurate location.

[Protective effects of total alkaloids from rhizoma Coptis chinensis on alcohol-induced gastric lesion in rats].

OBJECTIVE: To study the effects of total alkaloids(TA) from rhizoma Coptis chinensis on alcohol-induced gastric lesion in rats and the possible mechanisms. METHOD: The experimental gastric damges were established by intragastric(ig) absolute ethanol, and possible protective effects of TA given orally previously were evaluated by following parameters: gastric damage indexes, gastric juice volume, acidity, and mucus quantity. The contents of NO, MDA, *OH, and SOD activity were also measured in gastric mucosa. RESULT: TA showed significantly inhibitive effects on gastric damages induced by ig ethanol in a dose dependent manner. The effects of TA (120 mg x kg(-1)) were stronger than that of both cimitidine(70 mg x kg(-1)) and berberine(100 mg x kg(-1)), the quantity of later was equal to TA as calculated with berberine. TA significantly suppressed secretion of gastric acid caused by ethanol without clear influences on gastric juice volume and mucus secretion. TA obviously blunted ethanol-induced elevation of MDA and *OH, as well as decrease of NO level and SOD activity from gastric mucosa. CONCLUSION: It is suggested that the TA is a potent protective agent against ethanol-induced gastric damages. The mechanism of actions may be related with inhibiting the secretion of gastric acid and blunting the increase of MDA and *OH, as well as the decrease of NO level and SOD activity from gastric mucus.

Cardiac hypertrophy induced by prostaglandin F(2alpha) may be mediated by calcineurin signal transduction pathway in rats.

In this paper, we studied the relationship between the prostaglandin F(2alpha) (PGF(2alpha))-induced cardiac hypertrophy and calcineurin (CaN) signal transduction pathway in vivo and in vitro. Male Sprague-Dawley rats were given a single i.p. injection with monocrotaline (MCT) (60 mg/kg) and then given orally with celecoxib (20 mg/kg) or vehicle once a day for 14 d before (from d 1 to d 14) or after (from d 15 to d 28) right ventricular hypertrophy (RVH) was formed. Body weight (BW), right ventricular weight (RV), left ventricular with septum weight (LV), as well as lung weight were determined. RVH index (RVHI=RV/LV), RV/BW, and lung weight/BW were calculated and histological changes were observed with transmission electron microscope. PGF(2alpha) level, atrial natriuretic peptide (ANP) and CaN mRNA expressions, expression of CaN and its downstream effectors, NFAT(3) and GATA(4) protein were assayed by EIA kit, RT-PCR, and Western blotting, respectively. The cardiomyocyte hypertrophy in primary culture induced by PGF(2alpha) (0.1 micromol/L) was evaluated by measuring the cell diameter, protein content, and ANP mRNA as well as CaN mRNA expressions. It was found that 14 d or 28 d after MCT was given, the RVHI, RV/BW, and lung weight/BW were significantly increased by 47%, 53% and 118%, and by 64%, 94% and 156%, respectively; at the same time PGF(2alpha) levels in RV tissue were increased by 44% and by 51% with increasing RVHI, and elevated expressions of ANP and CaN mRNA, as well as CaN, NFAT(3) and GATA(4) proteins in a positive correlation manner. Furthermore, some histological injuries were found in RV tissue. Celecoxib, a cyclooxygenase inhibitor, obviously blunted the elevation of RVHI, RV/BW, and lung weight/BW no matter it was given before or after RVH. In vitro experiments showed that 0.1 micromol/L PGF(2alpha) significantly increased the cardiomyocyte diameter and protein content, and promoted ANP and CaN mRNA expressions, which was blocked by cyclosporin A, a CaN inhibitor. Our results indicate that PGF(2alpha) may be involved in cardiac hypertrophy induced by MCT in rats through CaN signal transduction pathway.

[The biochemical changes of hippocampus in patients before and after denture restoration: a preliminary 1H-magnetic resonance spectroscopy study].

OBJECTIVE: To study the effects of reconstruction of lost occlusal support on the biochemical changes of nervous system. METHODS: The changes of central nervous system metabolic compounds within hippocampus body were measured with proton magnetic resonance spectroscopy ((1)HMRS) before and after denture restoration (six weeks) in seven patients with prolonged loss of occlusal support. RESULTS: (1)HMRS indicated that Cho/Cr decreased by 11.9% (P < 0.05) six weeks after denture restoration, MI/Cr decreased by 28.8% (P < 0.05), and NAA/CR increased by 4.8% (P > 0.05) within hippocampus body. CONCLUSIONS: Recovery of occlusal support facilitates improvement of neuron functions in patients' hippocampus, which may help improve the functions of nervous system.