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Bacterial multi-drug resistance (MDR) is a global challenge in the fields of medicine and health, agriculture and fishery, ecology and environment. The cross-region spread of antibiotic resistance genes (ARGs) among different species is one of the main cause of bacterial MDR. However, there is no effective strategies for addressing the intensifying bacterial MDR. The CRISPR-Cas system, consisting of clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR associated proteins, can targetedly degrade exogenous nucleic acids, thus exhibiting high application potential in preventing and controlling bacterial MDR caused by ARGs. This review briefly introduced the working mechanism of CRISPR-Cas systems, followed by discussing recent advances in reducing ARGs by CRISPR-Cas systems delivered through mediators (e.g. plasmids, bacteriophages and nanoparticle). Moreover, the trends of this research field were envisioned, providing a new perspective on preventing and controlling MDR.
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Anti-Bacterial Agents , Bacteriophages/genetics , CRISPR-Cas Systems , Drug Resistance, Bacterial/genetics , Plasmids/geneticsABSTRACT
Objective: To observe the effects of electroacupuncture (EA) on uterine prostaglandin F2α (PGF2α), cyclooxygenase 2 (COX-2) and nuclear factor κB (NF-κB) in rats with primary dysmenorrhea (PD) and to discuss the possible mechanism in EA intervening PD. Methods: Forty Sprague-Dawley female rats were randomly divided into a blank group, a model group, an EA group and an ibuprofen group, with 10 rats in each group. The PD model was established using estradiol benzoate combined with oxytocin in the model group, EA group and ibuprofen group. At the same time of modeling, rats in the EA group were given EA at Guanyuan (CV 4) and Sanyinjiao (SP 6) once a day for 20 min each time for 10 consecutive days. Ibuprofen was intragastrically administered once a day for 10 consecutive days in the ibuprofen group. The same amount of normal saline was intragastrically administered once a day for 10 consecutive days in the blank group and model group. The number of writhing of rats in each group within 30 min was compared on the 11th day just after the interventions. The uterine homogenate supernatant was separated and the PGF2α level was detected by enzyme-linked immunosorbent assay. Western blot was applied for the detection of the expression levels of COX-2, phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues. Results: Compared with the blank group, the number of writhing in the model group increased significantly (P<0.01), and the expression levels of PGF2α, COX-2, phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues were significantly increased (all P<0.01). Compared with the model group, the number of writhing in the EA group and ibuprofen group were significantly reduced (both P<0.01), and the expression levels of PGF2α and COX-2 protein in uterine tissues were significantly reduced (both P<0.01). Compared with the model group, the phospho-NF-κB p65 level in uterine tissues in the EA group was significantly reduced (P<0.01). Compared with the ibuprofen group, the phospho-NF-κB p65 level in the EA group was significantly reduced (P<0.01). Conclusion: The mechanism of EA for PD rats may be related to inhibiting the phosphorylation of NF-κB and reducing the levels of COX-2 and PGF2α in uterine tissues.
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The present study was aimed to investigate the protective effect and anti-inflammation mechanism of astragaloside IV (AST-IV) on cerebral ischemia and reperfusion injury. Following the establishment of cerebral ischemia and reperfusion model in rats by modified suture method, neurological deficit scores and cerebral infarct volume were used to evaluate the pharmacological effect of AST-IV against cerebral ischemia-reperfusion injury. Western blot was used to detect the expression levels of NLRP3, pro-Caspase-1, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18, IL-18, phosphorylated and total nuclear factor kappa B (NF-κB)/p65 protein in the brain tissue. The results showed that compared with model group, the intervention of AST-IV decreased the neurological deficit scores, reduced the cerebral infarct volume, decreased the levels of NLRP3, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18 and IL-18, and inhibited the expression of phosphorylated NF-κB in brain tissue. The results suggest that AST-IV has a protective effect against cerebral ischemia and reperfusion injury, and its mechanism is related to inhibiting the phosphorylation of NF-κB and NLRP3 inflammasome activation.
Subject(s)
Animals , Rats , Brain Ischemia , Drug Therapy , Infarction, Middle Cerebral Artery , Drug Therapy , Inflammasomes , Metabolism , NF-kappa B , Metabolism , NLR Family, Pyrin Domain-Containing 3 Protein , Metabolism , Phosphorylation , Rats, Sprague-Dawley , Reperfusion Injury , Drug Therapy , Saponins , Pharmacology , Triterpenes , PharmacologyABSTRACT
Objective: To observe the effect of electroacupuncture (EA) on nuclear factor kappa B (NF-κB) and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in uterine tissues of rats with primary dysmenorrhea (PD), thus to explore the possible mechanism of EA for PD. Methods: Fifty female Sprague-Dawley (SD) rats were randomly divided into a normal group, a model group, an EA at non-acupoint group, an EA at acupoint group and a Western medicine group, with 10 rats in each group. Except for the normal group, rats in the other four groups were treated with estradiol benzoate combined with oxytocin for 11 d to establish PD rat models. From day 1 of the modeling, rats in the normal group and the model group were only properly grasped without any intervention; Guanyuan (CV 4) and Sanyinjiao (SP 6) were selected for EA treatment in the EA at acupoint group; rats in the EA at non-acupoint group were treated with EA at 5 mm away from the acupoints selected above; rats in the Western medicine group were treated with ibuprofen via gavage. Rats in each group were treated for 10-day successively. On the 11th day, except for the normal group, rats in the other groups were intraperitoneally injected with oxytocin (2 U/rat), and the writhing number within 30 min in each group was compared; the pathological changes in rat uteruses were observed by hematoxylin-eosin (HE) staining, and the pathological damage scores were evaluated. Protein expression levels of NF-κB p65, phospho-NF-κB p65, NLRP3, cysteine aspastic acid-specific protease 1 (caspase-1), interleukin (IL)-1β and IL-18 were detected by Western blot. Results: Compared with the normal group, the writhing number increased significantly (P<0.05), and the extensive exfoliation of the endometrium, severe edema, and histopathological score all increased significantly in the model group (P<0.05) as well as the protein levels of NLRP3, caspase-1, IL-1β and IL-18, and the ratio of phospho-NF-κB p65/NF-κB p65 in rat uterine tissues (all P<0.05); compared with the model group, the numbers of writhing reaction decreased within 30 min (P<0.05), the endometrial exfoliation was rare, the edema degree was mild, and the histopathological scores decreased significantly (all P<0.05) in the EA at acupoint group and the Western medicine group; compared with the model group, the phospho-NF-κB p65/NF-κB p65 ratio and the NLRP3, caspase-1, IL-1β and IL-18 protein levels of rat uterine tissues in the EA at acupoint group were significantly lower (P<0.05); compared with the model group, the caspase-1, IL-1β and IL-18 protein levels of the rat uterine tissues decreased significantly (all P<0.05), and the differences in the NLRP3 and phospho-NF-κB p65/NF-κB p65 levels were statistically insignificant (all P>0.05) in the Western medicine group; compared with the Western medicine group, the phospho-NF-κB p65/NF-κB p65 ratio, also the NLRP3, IL-1β and IL-18 protein levels of the uterine tissues decreased significantly in the EA at acupoint group (all P<0.05), while the difference in the caspase-1 level was statistically insignificant (P>0.05); there were no significant differences between the EA at non-acupoint group and the model group in any indicators (all P>0.05). Conclusion: EA at acupoints significantly improves the pain and pathological damages of PD rats. The mechanism may be related to the reduced uterine inflammation via inhibiting NF-κB phosphorylation and NLRP3 activation in uteruses of PD rats.
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Pyroptosis is a form of inflammatory programmed cell death activated by caspase-1 and caspase-4/5/11, and involves in the pathogenesis of infectious diseases and nervous system diseases. Pyroptosis is mediated by canonical inflammasome pathway and non-canonical inflammasome pathway. The canonical inflammasome pathway is activated in stroke and aggravates brain injury. Inhibition of inflammasome, caspase-1, IL-1β and IL-18 ameliorates brain injury. These studies indicate that canonical inflammasome pathway contributes to post-stroke brain injury, therefore, pyroptosis has become a potential therapeutic target for preventing excessive cell death during stroke. We reviewed the relationship between pyroptosis and stroke to provide some perspectives on future researches in this field.
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Objective: To characterize the “multi-components, multi-targets, and multi-pathways” mechanism of Jiangzhi Ligan Decoction on non-alcoholic fatty liver disease (NAFLD) using network pharmacology technology. Methods: Data regarding natural molecules of Jiangzhi Ligan Decoction, targets of NAFLD, and interactions between natural molecules and NAFLD targets were screened. Network pharmacology of the interactions between natural molecules and NAFLD targets were established using Cytoscape software. The biological process and the signaling pathway of the putative targets were analyzed using ClueGO. Results: The network analysis indicated that 82 active ingredients and 53 NAFLD related targets were screened in Jiangzhi Ligan Decoction, which was involved in regulation of insulin resistance, oxidative stress, inflammation, PI3K/Akt signaling pathway, inflammasome signaling pathway, IL-10 signaling pathway, and T cell signaling pathway. Conclusion: This study provides an important basis for further study on the pharmacological mechanism of Jiangzhi Ligan Decoction in the treatment of non-alcoholic fatty liver disease.
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The aim is to study the effect of astragaloside Ⅳ (AST Ⅳ) combined with Panax notoginseng saponins (PNS) on cerebral ischemia-reperfusion injury, and to probe the synergistic mechanism through the pharmacokinetics of the four major components such as AST Ⅳ, ginsenoside Rg₁ (Rg₁), ginsenoside Rb₁ (Rb₁), notoginsenoside R₁ (R₁) in cerebral ischemia-reperfusion rats. Following the establishment of cerebral ischemia/reperfusion model in rats by modified suture method, neurological function score, cerebral infarction area and pathomorphology were used to evaluate the pharmacological effect that the combination of AST Ⅳ and PNS antagonized cerebral ischemia-reperfusion injury; the contents of AST Ⅳ, Rg₁, Rb₁, R₁ in rat plasma of different time points were determined with ultra performance liquid chromatography tandem massspectrometry (UPLC-MS/MS), pharmacokinetic parameters were calculated and pharmacokinetics changes of the main effective components were analyzed. The results showed that AST Ⅳ, PNS alone and their combination could reduce the cerebral infarction area of rats, relieve the behavioral scores of neurologic deficit, improve the pathological changes after cerebral ischemia, the effects of the combination were better. Among AST Ⅳ, Rg₁, Rb₁, R₁, the area under the curve (AUC) was significantly increased, the mean residence time of (MRT0-t) was delayed, the peak concentration (Cmax) was significantly raised, the apparent volume of distribution (Vz/F) was reduced, and the clearance rate in vivo was significantly slowed. It suggested that AST Ⅳ combined with PNS has synergistic enhancement on anti-cerebral ischemia/reperfusion injury, moreover, make the pharmacokinetic behavior of the main effective components change, the mechanism may be associated with prolonging the retention time of the effective components in cerebral ischemia condition, elevating the bioavailability.
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Objective To investigate the predisposing factors and clinical features of disseminated herpes zoster, and to explore factors influencing postherpetic neuralgia. Methods Clinical data were collected from 53 patients with disseminated herpes zoster and 809 patients with common herpes zoster between 2012 and 2015, and analyzed retrospectively. Logistic regression analysis was used to assess factors influencing the occurrence of and pain intensity in disseminated herpes zoster, as well as the occurrence of postherpetic neuralgia. Results No significant difference in patients′age was observed between the disseminated and common herpes zoster groups(56.66 ± 17.24 vs. 56.50 ± 15.51 years, t=0.071, P>0.05), but there was a significant difference in the gender ratio between the two groups(χ2 = 8.16, P = 0.004). The incidence rates of bullae, pustules and fever were all significantly higher in the disseminated herpes zoster group than in the common herpes zoster group(15.09%vs. 3.58%,χ2=16.04, P<0.01;47.17%vs. 26.82%,χ2=10.20, P<0.01;30.19%vs. 8.03%,χ2=28.68, P<0.01). The disseminated herpes zoster group also showed significantly higher pain scores at admission compared with the common herpes zoster group (Median[P25- P75]: 6[4- 7.5] vs. 5[3- 7], Z =-3.460, P = 0.001). Logistic regression analysis revealed that gender, age, fatigue and HIV infection were significantly associated with the occurrence of disseminated herpes zoster (all P<0.05). Additionally, HIV infection(OR=5.570, 95%CI:1.196-25.939, P=0.029), gender(OR=0.166, 95%CI:0.029-0.945, P=0.043), age(OR=1.064, 95%CI:1.010-1.119, P=0.019)and the number of days that antiviral therapy lasted(OR=0.669, 95%CI:0.505-0.885, P=0.005)were all factors influencing the occurrence of postherpetic neuralgia. Conclusion Male, old age, fatigue and especially HIV infection are risk factors for the occurrence of disseminated herpes zoster, and male, old age and antiviral therapy duration may be associated with the occurrence of postherpetic neuralgia.
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Objective To observe the analgesic and anti-inflammatory effects of the water extract of Glycosmis citrifolia (Willd.) Lindl.on mice and explore the mechanism. Methods The analgesic and anti-inflammatory effects were evaluated by 0.7% acetic acid-induced writhing test,the hot plate test,tests of dimethylbenzene-induced ear swelling,1% carrageenan-induced paw edema,determination of PGE2 in inflammatory feet,0.6% acetic acid-induced increase in peritoneal capillary permeability and cotton ball granuloma. Results The water extract of Glycosmis citrifolia (Willd.) Lindl.at low,medium and high doses can reduce the acetic acid-induced writhing times (P<0.01 or P<0.05),increase the pain threshold of mice (P<0.01 or P<0.05), inhibit dimethylbenzene-induced ear swelling (P<0.01 or P<0.05),1% carrageenan-induced paw edema (P<0.01 or P<0.05) and PGE2 production (P<0.01),0.6% acetic acid-induced increase of peritoneal capillary permeability (P<0.05),and the de-velopment of cotton ball granuloma (P<0.01 or P<0.05). Conclusion The water extract of Glycosmis citrifolia (Willd.) Lindl.shows analgesic and anti-inflammatory effects on mice.
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Objective To investigate the effect and safety of primary percutaneous coronary intervention (PCI) of acute ST-segment elevation myocardial infarction (STEMI) in elderly patients.Methods 103 consecutive patients with STEMI treated by primary PCI were divided into two groups according to the age:the elderly group [aged≥65 years,with a mean age of (75.7 ±6.2) years(n =49],the non-elderly group [aged＜65 years,with a mean age of (43.0±8.6) years(n =54].Clinical characteristics,complications related to PCI procedure and success rate were analyzed,and major cardiovascular events (MACE) were followed up for(5.7 ± 1.2) months.Results The proportion of female,patients with Killip ≥ Ⅲ,three vessels disease and higher level of serum brain natriuretic peptide were higher in elderly group than in non-elderly group (all P＜0.05).No significant difference was observed between the two groups in success rate and complications of PCI procedure (both P＞0.05).Patients were followed up for (5.7± 1.2) months.The in-hospital and one-month mortalities were higher in elderly group than in non-elderly group [8.2％ (4 cases)vs.0％ (0 case),10.2％(5 cases) vs.0 ％ (0 case),respectively,all P＜0.05].There was no significant difference in six-month mortality and MACE between the two groups.Multivariate logistic regression analysis showed that Killip ≥ Ⅲ was related with the increase of one-month mortality in patients with STEMI undergoing primary PCI,whereas age was not.Conclusions Primary PCI is effective and safe in elderly patients with STEMI.
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Objective To investigate the expression and clinical significance of lipoxin A4,leukotrienc C4,lipoxygenase-5 in peripheral blood of pregnant women with different types of severe preeclampsia.Methods Forty-five singleton pregnant women who accepted antenatal care and delivered in First Affiliated Hospital of Wenzhou Medical College were enrolled in this study from December 2010 to June 2011.All objects were divided into normal pregnancy group (n=20),early onset severe preeclampsia group (n=10) and late onset severe preeclampsia group (n=15).Enzymelinked immunosorbent assay was used to detect lipoxin A4 and leukotriene C4 levels in peripheral blood.The level of lipoxygenase-5 mRNA in white blood cells was detected by real time fluorescence quantitative reverse transcription-polymerase chain reaction.The differences of lipoxin A4,leukotriene C4 and lipoxygenase-5 mRNA among groups were compared by analysis of variance and LSD-t test;and correlations among their expressions were analyzed by linear regression.Results Lipoxin A4 level in early and late onset severe preeclampsia group was (355.3±116.0) pg/ml and (389.7±117.5) pg/ml,which were both significantly lower than that in normal pregnancy group [(555.0±139.8) pg/ml] (t=-4.03 and-3.77,P＜0.05 respectively).The leukotriene C4 level in early and lateonset severe preeclampsia and normal pregnaney group was (591.3±185.5) pg/ml,(510.3±197.1) pg/ml and (496.9 ± 158.8) pg/ml,no statistical difference were found (F=0.889,P＞0.05) ; neither did the expression of lipoxygenase 5 mRNA,which was 4.2± 1.9 in normal pregnancy group,4.8 ± 2.0 in early onset severe preeclampsia group and 4.4 ± 1.2 in late onset severe preeclampsia group (F=0.311,P＞0.05).There was no correlation among the levels of lipoxin A4,leukotriene C4 and lipoxygenase-5 mRNA in each group (P ＞ 0.05).Conclusions Early and remarkable decreasing of lipoxin A4 level might contribute to the development of early onset severe preeclampsia.
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ObjectiveTo investigate the effects of 5(S),6(R),7-trihydroxyheptanoic acid methyl ester (BML-111) on pregnant mice with fetal growth restriction(FGR) induced by antenatal dexamethasone and its probable mechanism. MethodsThe mice were mated overnight,with day 1 of pregnancy designated as the day on which spermatozoa were presented in a vaginal smear.The pregnant mice were then randomly divided into control group,dexamethasone group and BML-111 group.From 9 to 14 days of pregnancy,pregnant ICR mice of control,dexamethasone and BML-111 group were treated separately with saline,dexamethasone(5 mg/kg) and dexamethasone at 8:00 am,and two hours later they were treated separately again with 1 mg/kg saline,saline and BML-111.On the day 18 of gestation,they were sacrificed after blood were collected from their eyeballs.The serum lipoxin A4 was measured with enzyme-linked immunosorbent assay. Fetuses were delivered by cesarean section; the placenta and uterus were immediately removed and frozen.Gene expressions of 11β-hydroxysteroid dehydrogenase 2 ( 11β-HSD2 ),interleukin-1β (IL-1β) in placenta and lipoxin A4 receptor-formyl peptide receptor 3 (FPR3)in uterine were detected by reverse transcriptionpolymerase chain reaction and compared with analysis of variance.The 11β-HSD2 protein in mice placenta was detected by immunohistochemistry. ResultsThe mean fetal weight of dexamethasone group was (0.823±0.054) g,lower than that of the control group and BML-111 group [(1.103±0.218) g and (0.992 ± 0.207) g] (t =- 4.108 and - 2.890,P ＜ 0.05 respectively).Protein expression of 11β-HSD2 in dexamethasone group (0.030±0.019) was weaker than that in control group (0.058±0.015,t=-3.107,P＜0.05) or in BML-111 group (0.049±0.026,t=-2.211,P＜0.05).The expression of 11β-HSD2 mRNA in dexamethasone group (0.457±0.062) was lower than that in control group (0.943±0.057,t=-9.418,P＜0.05) or in BML-111 group (0.698±0.071,t=-4.617,P＜0.05).Expression of IL-1β mRNA in dexamethasone group (0.543±0.103)was less than that in control group (0.710± 0.085,t=-3.736,P＜0.05) but more than that in BML-111 group (0.229 ±0.031,t=7.025,P＜0.05). The expression of FPR3 mRNA in dexamethasone group (0.323 ± 0.019) was less than that in control group (0.857 ± 0.057,t =-14.630,P＜0.05) or in BML-111 group (0.499 ±0.050,t=-4.822,P＜0.05).The serum concentration of lipoxin A4 in dexamethasone group was lower than that in control group [(64.463±22.144) pg/ml vs (101.610±24.916) pg/ml,t=3.152,P＜0.05].ConclusionsBML-111 regulate the expression of 11β-HSD2 and then protect against FGR resulted from too much prenatal application of dexamethasone.
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<p><b>OBJECTIVE</b>To evaluate four candidate variable number tandem repeat (VNTR) loci for genotyping Mycobacterium tuberculosis complex strains.</p><p><b>METHODS</b>Genomic sequences for two M. tuberculosis strains (CCDC5079 and CCDC5180) were generated, and using published sequence data, four candidate VNTR loci were identified. The VNTRs were used to genotype 225 Chinese clinical M. tuberculosis complex strains. The discriminatory power of the VNTRs was evaluated using BioNumerics 5.0 software.</p><p><b>RESULTS</b>The Hunter-Gaston Index (HGI) for BJ1, BJ2, BJ3, and BJ4 loci was 0.634, 0.917, 0.697, and 0.910, respectively. Combining all four loci gave an HGI value of 0.995, thus confirming that the genotyping had good discriminatory power. The HGI values for BJ1, BJ2, BJ3, and BJ4, obtained from Beijing family strain genotyping, were 0.447, 0.878, 0.315, and 0.850, respectively. Combining all four loci produced an HGI value of 0.988 for genotyping the Beijing family strains. We observed unique patterns for M. bovis and M. africanum strains from the four loci.</p><p><b>CONCLUSION</b>We have shown that the four VNTR loci can be successfully used for genotyping M. tuberculosis complex strains. Notably, these new loci may provide additional information about Chinese M. tuberculosis isolates than that currently afforded by established VNTR loci typing.</p>
Subject(s)
Humans , Cluster Analysis , Genotyping Techniques , Minisatellite Repeats , Mycobacterium bovis , Genetics , Mycobacterium tuberculosis , GeneticsABSTRACT
Objective To explore lipoxinA4 (LXA4) expression in maternal serum of pregnant women and the protective effect and mechanism of LXA4 on trophoblastic cells from oxidative injury. Methods Trophoblastic cells were randomized into six groups: Control group; Lipopolysaccharides (LPS) group, cells were stimulated by 10 μg/ml LPS for 24 h; Intervention group, cells stimulated by LPS were treated with 100 nmol/L LXA4 for 24 h; LXA4 group, cells were treated with 100 nmol/L LXA4 for 24 h; Antagonistic group, cells stimulated by LPS were treated with 100 nmol/L LXA4 plus 100 μmol/L N-tert-butoxycarbonyl-2-pyrrolidine (BOC-2) for 24 h; BOC-2 group, trophoblastic cells stimulated by LPS were treated with 100 μmol/L BOC-2 for 24 h. The serum concentration of LXA4 in normal group and preeclampsia group was detected by ELISA. The intracellular formation of reactive oxygen species (ROS) was detected by 2,7-dichlorofluorescein diacetate (DCFH-DA) as a fluorescent probe. SOD mRNA was analyzed by RT-PCR. SOD and Nrf2 protein expressions were analyzed by Western blot. The levels of SOD in trophoblastic cells were detected by using detection kit. Results (1) The serum concentration of LXA4 was significantly lower in preeclampsia group (165.53±18.89) pg/L than in the control [(545.67±30.91) pg/L, P0.05). Conclusions LXA4 can significantly reduce the oxidative stress of placental trophoblastic cells stimulated by LPS. LXA4 can bind to lipoxin receptors and activate Nrf2-ARE signaling pathway playing a protective effect. So LXA4 in pregnant women can affect the oxidative stress of placenta.
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<p><b>BACKGROUND</b>Recent studies suggest that bone marrow adipose tissue might play a role in the pathogenesis of osteoporosis. There are inconsistent findings on the relationship among marrow fat content, bone mineral density and apparent diffusion coefficient (ADC). This study aimed to prospectively explore the efficacy of MR spectroscopy (MRS) and diffusion-weighted MR imaging (DWI) in detecting vertebral marrow changes in postmenopausal women with varying bone densities.</p><p><b>METHODS</b>Both MRS and DWI of the lumber spine were performed in 102 postmenopausal women (mean age, (67.3 +/- 6.5) years; range, 55 - 83 years), who underwent dual X-ray absorptiometry. Marrow fat content and ADC were compared and correlated among three groups: 24 with normal bone density, 31 with osteopenia and 47 with osteoporosis.</p><p><b>RESULTS</b>Vertebral marrow fat content was significantly increased in the osteoporotic group ((65.60 +/- 7.68)%, P < 0.001) and the osteopenic group ((57.68 +/- 6.45)%, P < 0.001), when compared with the normal bone density group ((51.67 +/- 3.27)%). ADC values were significantly decreased in the osteoporotic group ((0.39 +/- 0.03) x 10(-3)mm(2)/s, P < 0.001) and in the osteopenic group ((0.42 +/- 0.02) x 10(-3)mm(2)/s, P < 0.001), when compared with the normal bone density group ((0.47 +/- 0.03) x 10(-3)mm(2)/s). The marrow fat content negatively correlated with both bone density (r = -0.731, P < 0.001) and marrow ADC (r = -0.572, P < 0.001). The bone density positively correlated with the ADC values (r = 0.802, P < 0.001).</p><p><b>CONCLUSIONS</b>Postmenopausal women experience a corresponding increase in vertebral marrow fat content as the bone density decreases. Marrow fat content and ADC correlate to the bone density. MRS and DWI may indirectly assess the early bone marrow changes in postmenopausal women.</p>