[Expression and significance of hypoxia-inducible factor-1α and vascular endothelial growth factor and receptor 2 in stage 3 pressure injury of rats].

OBJECTIVE: To analyze the expression and relationship of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF) and kinase insert domain receptor (KDR) in local skin tissues of pressure injury and investigate the possible mechanism of stage 3 pressure injury refractory wound. METHODS: Forty male SD rats were randomly divided into normal control group, compressed 3 d, 5 d, 7 d, and 9 d groups. Stage 3 pressure injury animal model were established by magnet compression. The morphology of skin was observed by HE staining. The expression of VEGF was detected by immunohistochemistry. The expression levels of HIF-1α, VEGF and KDR protein in skin tissue were detected by Western blot. One-way analysis of variance and LSD test were performed on the data. RESULTS: ①The HE results showed that compared with the normal control group, the epidermis of the compressed group was gradually thickened, the number of blood vessels was decreased, the collagen arrangement disordered and inflammatory cells infiltration were increased. ②Immunohistochemical results showed that the expression of VEGF protein in the 3 d group was significantly higher than that in the normal control group (P＜0.01). The expression of VEGF protein in the skin tissue of 5 d, 7 d and 9 d groups was lower than that in normal control group (P＜0.05). WB results were consistent with immunohistochemistry results. ③WB results showed that the expression of HIF-1α in the skin tissues of the rats in 3 d, 5 d and 7 d groups was higher than that in the normal control group (P＜0.01 or P＜0.05). The expression of KDR protein was lower than that of the normal control group (P＜0.05 or P＜0.01). CONCLUSION: HIF-1α mediated reduction of VEGF and KDR protein expression and decreased tissue angiogenesis may be one of the important causes of chronic dysfunction of stage 3 pressure injury.

The Cardioprotective Effects of Remote Ischemic Conditioning in a Rat Model of Acute Myocardial Infarction.

BACKGROUND Cardiac remote ischemic conditioning (RIC) is a noninvasive cardioprotective method in ischemia-reperfusion injury and acute myocardial infarction (AMI). The aims of this study were to investigate the effects of RIC in a rat model of AMI. MATERIAL AND METHODS Adult male Sprague-Dawley rats included the AMI group that underwent ligation of the left anterior descending (LAD) coronary artery (n=24), the RIC group that consisted the AMI rat model treated with RIC once daily in the left hind limb until days 1, 7 and 14 (n=24), and the sham group (n=24). Myocardial infarct size was measured by routine histology with triphenyltetrazolium chloride (TTC) and Masson's trichrome histochemical staining for myocardial necrosis and fibrosis, respectively. Serum levels of Bcl-2, Bax, caspase-3, and inducible nitric oxide synthase (iNOS) were measured by enzyme-linked immunosorbent assay (ELISA). The apoptosis index was detected using the TUNEL assay. Spectrophotometry of the myocardium was used to identify mitochondrial complexes and myocardial ATP. RESULTS The RIC group showed improved cardiac hemodynamics, reduced the size of the myocardial infarction, upregulated expression of Bcl-2, and down-regulation of the levels of Bax, caspase-3, and iNOS, and reduced cardiac myocyte apoptosis and inhibited the opening of the mitochondrial permeability transition pore (MPTP). CONCLUSIONS In a rat model of AMI, RIC improved the hemodynamic index, reduce the levels of apoptosis and myocardial injury, and improved mitochondrial function.

Novel synthesized zinc oxide nanoparticles loaded alginate-chitosan biofilm to enhanced wound site activity and anti-septic abilities for the management of complicated abdominal wound dehiscence.

Wound dehiscence is a surgical complication and its management is inevitable because 25% to 35% of patients suffered from post laparotomy wound dehiscence. The excellent biodegradability and biocompatibility of chitosan and alginate have provided ample space for future developments in biomedical applications. Hence, the present work is directed towards the synthesis of robust biofilm made up of chitosan (CS), zinc oxide (ZnO) nanoparticles and Alginate (Alg). Chitosan and alginate were used for their pore forming ability, and ZnO is for its antibacterial action. The proposed biofilm was characterized with different characterization techniques such as Fourier Transform Infrared (FTIR) spectroscopy, UV-vis spectroscopy, X-ray Diffraction (XRD), Scanning Electron Microscopy (SEM) and Transmission Electron microscopy (TEM) analyses. FTIR results inferred the strong interaction between the three components. The surface morphology of ZnO-CS/Alg. biofilm was exhibited as the spherical shaped nanoparticles which are firmly anchored on the polymer matrix. TEM analysis also confirmed the formation of biofilm. The XRD analysis confirmed the presence of ZnO in the biopolymer. The line broadening suggests that the crystallize size is in few nanometers. The average crystallite size was estimated as 50 nm using Scherrer formula. The antibacterial activity of the biofilm was successfully established against bacterial pathogens. Therefore, the developed materials have a potential play as antimicrobial role for the abdominal wound healing and biomedical fields.

The effect of cassia seed extract on the regulation of the LKB1-AMPK-GLUT4 signaling pathway in the skeletal muscle of diabetic rats to improve the insulin sensitivity of the skeletal muscle.

BACKGROUND: This study aimed to observe the hypoglycemic effect of cassia seed extract in rats with type-2 diabetes mellitus and its effect on reducing insulin resistance in the skeletal muscle. METHODS: 50 rats were randomly divided into the normal, model, high-dose, middle-dose, and low-dose groups of cassia seed extract (n = 10 each). A high-fat diet combined with streptozotocin administration was adopted to build type 2 diabetes models. The cassia seed extract groups were fed different concentrations cassia seed extract while the normal and model groups were fed the same volume of normal saline. The weight, FINS, GIR, insulin tolerance, blood glucose and blood lipid level, oxidative stress indices and expressions related to the LKB1-AMPK-GLUT4 pathway were detected and compared between the two groups. RESULTS: Compared with the normal group, the model group showed lower weight, glucose infusion rate and expressions related to LKB1-AMPK-GLUT4 pathway and higher FINS, insulin tolerance, blood glucose and blood lipid level and oxidative stress indices (all P < 0.05). Compared with the model group, higher weight, glucose infusion rate and expressions related to LKB1-AMPK-GLUT4 pathway and lower FINS, insulin tolerance, blood glucose and blood lipid level and oxidative stress indices were observed in all groups that were administered cassia see extract (all P < 0.05). CONCLUSION: Cassia seed extract could noticeably improve the insulin resistance of diabetic rats and enhance the insulin sensitivity of their skeletal muscles. Its mechanism may be related to damage repair of the LKB1-AMPK-GLUT4 signaling pathway and oxidative stress in the skeletal muscle.

[Anti-arrhythmic effects of taurine-magnesium coordination compound on torsades de pointes].

OBJECTIVES: To investigate the effect of taurine magnesium coordination compound (TMCC) on torsades de pointes (TdP) in isolated guinea pig hearts. METHODS: Healthy male guinea pigs weighting 250~300 g were randomly divided into 4 groups:①TdP model group (n=7):Isolated hearts were perfused by normal K-H solution 20 minutes, then perfused by slowly activated delayed rectifier potassium current(IKs) blocker 10µmol/L Chromanol 293B under hypokalemic solution(1.8 mmol/L) to establish TdP model;②~④ TdP model + TMCC group (n=6):Isolated hearts were perfused by normal K-H solution for 20 minutes, then perfused by IKs blocker 10µmol/L Chromanol 293B under hypokalemic solution(1.8 mmol/L) for 60 minutes, at the same time TMCC which concentration was 1, 2, 4 mmol/L was administered respectively by Langendorff retrograde aortic perfusion method. Cardiac surface electrocardiogram of guinea pigs in vitro was collected and recorded by Biopac electrophysiological recorder. Incidence of TdP, transmural dispersion of repolarization (TDR), instability of QT interval were acquired from Lead Ⅱ electrocardiograph (ECG) wave forms to describe the effect of TMCC on TdP model. Datas were acquired at the time of 20 min and pre-TdP, in case there was no TdP observed, a value of 60 min was entered for calculation purpose. RESULTS: Incidence of TdP in TdP model group was 6/7. TdP incidence could be decreased significantly by 1, 2, 4 mmol/L TMCC, and was 5/6, 1/6, 0/6 respectively. Compared with the pre-drug, Chromanol 293B under hypokalemic solution in TdP model group increased TDR(corrected) evidently(P<0.01). Compared with the pre-drug, 1, 2, 4 mmol/L TMCC in TdP model + TMCC group could decrease the increased TDR(corrected) induced by Chromanol 293B under hypokalemic solution(P>0.05). Compared with the TdP model group, 2, 4 mmol/L TMCC could evidently decrease the instability of QT interval induced by Chromanol 293B under hypokalemic solution(P<0.05). During the establishment of TdP model, P waves in more than one cardiac cycle continuously were disappeared in ECG. However, P wave could always be seen independent in ECG acquired from TdP model + TMCC group. CONCLUSIONS: TMCC can play the role against TdP through decreasing TDR and instability of QT interval, and inhibiting early after depolarization(EAD).

Therapeutic effects of a taurine-magnesium coordination compound on experimental models of type 2 short QT syndrome.

Short QT syndrome (SQTS) is a genetic arrhythmogenic disease that can cause malignant arrhythmia and sudden cardiac death. The current therapies for SQTS have application restrictions. We previously found that Mg· (NH2CH2CH2SO3)2· H2O, a taurine-magnesium coordination compound (TMCC) exerted anti-arrhythmic effects with low toxicity. In this study we established 3 different models to assess the potential anti-arrhythmic effects of TMCC on type 2 short QT syndrome (SQT2). In Langendorff guinea pig-perfused hearts, perfusion of pinacidil (20 µmol/L) significantly shortened the QT interval and QTpeak and increased rTp-Te (P<0.05 vs control). Subsequently, perfusion of TMCC (1-4 mmol/L) dose-dependently increased the QT interval and QTpeak (P<0.01 vs pinacidil). TMCC perfusion also reversed the rTp-Te value to the normal range. In guinea pig ventricular myocytes, perfusion of trapidil (1 mmol/L) significantly shortened the action potential duration at 50% (APD50) and 90% repolarization (APD90), which was significantly reversed by TMCC (0.01-1 mmol/L, P<0.05 vs trapidil). In HEK293 cells that stably expressed the outward delayed rectifier potassium channels (IKs), perfusion of TMCC (0.01-1 mmol/L) dose-dependently inhibited the IKs current with an IC50 value of 201.1 µmol/L. The present study provides evidence that TMCC can extend the repolarization period and inhibit the repolarizing current, IKs, thereby representing a therapeutic candidate for ventricular arrhythmia in SQT2.

Effects of non-invasive remote ischemic conditioning on rehabilitation after myocardial infarction.

Recent studies have demonstrated that remote ischemic conditioning (RIC) creates cardioprotection against ischemia/reperfusion injury and myocardial infarction (MI); however, the effects of non-invasive remote ischemic conditioning (nRIC) on prognosis and rehabilitation after MI (post-MI) remain unknown. We successfully established MI models involving healthy adult male Sprague-Dawley rats. The nRIC group repeatedly underwent 5 min of ischemia and 5 min of reperfusion in the left hind limb for three cycles every other day until weeks 4, 6, and 8 after MI. nRIC improved cardiac hemodynamic function and mitochondrial respiratory function through increasing myocardial levels of mitochondrial respiratory chain complexes I, II, III, IV, and adenosine triphosphate (ATP) and decreasing the activity of nitric oxide synthase (NOS). nRIC could inhibit cardiomyocytes apoptosis and reduce myocardium injury through raising the expression of Bcl-2 and reduced the content of creatine kinase-MB, cardiac troponin I and Bax. The results indicated that long-term nRIC could accelerate recovery and improve prognosis and rehabilitation in post-MI rats.

[Effects and mechanism of bFGF on rat myoblast oxidative injury induced by hydrogen peroxide].

OBJECTIVE: To explore the protective role of basic fibroblast growth factor (bFGF) on attenuating hydrogen peroxide-induced injury in cultured rat myoblasts. METHODS: Cultured rat myoblasts at growth phase were randomly divided into four groups (n=6):control group (control), bFGF group (bFGF), model group(H2O2) and the treatment group (bFGF + H2O2). Model group was treated with 100 µmol/L hydrogen peroxide for 4h. B-cell lymphoma-2 (Bcl-2) positive particles were detected by immunohistochemistry; Reactive oxygen species (ROS) and expression for Bcl-2 associated X protein (Bax), Bcl-2 and Cytochrome C (Cyt. C) fluorescence were observed under the invented microscope; Cyt. C and Poly ADP-ribose polymerase(PARP)protein were assessed by Western blot. RESULTS: Compared with control group, the myoblats in the model group showed low expression of Bcl-2 positive particles, accompanied by high expression of ROS level and Cyt. C fuorescence (P < 0.05); Compared with model group, bFGF enhanced Bcl-2 activity of the myoblasts, and significantly downregulated Cyt. C and PARP expression (P < 0.05). CONCLUSIONS: bFGF could attenuate oxidative injury of rat myoblasts induced by hydrogen peroxide, which mechanism might be related to enhanced Bcl-2 and reduced ROS, Cyt. C levels.

Pressure Combined with Ischemia/Reperfusion Injury Induces Deep Tissue Injury via Endoplasmic Reticulum Stress in a Rat Pressure Ulcer Model.

Pressure ulcer is a complex and significant health problem in long-term bedridden patients, and there is currently no effective treatment or efficient prevention method. Furthermore, the molecular mechanisms and pathogenesis contributing to the deep injury of pressure ulcers are unclear. The aim of the study was to explore the role of endoplasmic reticulum (ER) stress and Akt/GSK3ß signaling in pressure ulcers. A model of pressure-induced deep tissue injury in adult Sprague-Dawley rats was established. Rats were treated with 2-h compression and subsequent 0.5-h release for various cycles. After recovery, the tissue in the compressed regions was collected for further analysis. The compressed muscle tissues showed clear cellular degenerative features. First, the expression levels of ER stress proteins GRP78, CHOP, and caspase-12 were generally increased compared to those in the control. Phosphorylated Akt and phosphorylated GSK3ß were upregulated in the beginning of muscle compression, and immediately significantly decreased at the initiation of ischemia-reperfusion injury in compressed muscles tissue. These data show that ER stress may be involved in the underlying mechanisms of cell degeneration after pressure ulcers and that the Akt/GSK3ß signal pathway may play an important role in deep tissue injury induced by pressure and ischemia/reperfusion.

[The role of cell apoptosis mediated by endoplasmic reticulum stress (ERS) of deep tissue injury of pressure ulcer of rats].

OBJECTIVE: To observe the the expression of endoplasmic reticulum stress (ERS) related factors in deep tissue injury (DTI) at pressure ulcer rat and to investigate the ERS mechanism of DTI in muscle tissue and protective effect of 4-phenylbutyric acid (4-PBA) in local tissue. METHODS: Fifty male SD rats were randomly devided into control group, model group, experimental group NS group and PBA group, the experimental groups were divided into 4 d, 7 d, 14 d and 21 d group according to the observation time (n = 5). Rats in the PBA group were administrated with gastric perfusion of 4-PBA after the modeling; the NS group was given normal saline of the same quantity. Using HE staining to observe morphologic character. The expression of glucose regulated protein 78 (GRP78), CHOP, Caspase 12 were detected by immunohistochernical staining. Cell apoptosis was detected by TUNEL assay. RESULTS: HE staining results showed that each group demonstrated compression injury compared with control group: cellular swelling, ompaction of nuclear, and apoptosis in muscle tissue. The new muscle fiber in 4-PBA group fused faster than those in NS group. The number of TUNEL positive cells peaked at 4 day after compression, then got decreased on day 7 in muscle tissue, apoptosis positive cells were diminished after 4-PBA treatment. The immunohistochemical staining results showed that the expression of protein GRP78, CHOP, Caspase 12 peakd 4 d after modeling and decreased gradually. The GRP78, CHOP, Caspase 12 protein expression were significantly higher than those of PBA group at all time points (P < 0.05). CONCLUSION: Cell apoptosis induced by endoplasmic reticulum stress took part in deep tissue injury resulting of pressure ulcer, which mechanism might be related to reducing apoptosis mediated by CHOP, Caspase 12.

[Effects of endoplasmic reticulum stress related proteins and their mediated apoptosis in the formation of deep tissue injury of pressure ulcer in rats].

OBJECTIVE: To explore the effects of endoplasmic reticulum stress (ERS) related proteins and their mediated apoptosis in the formation of deep tissue injury of pressure ulcer in rats. METHODS: Forty male Sprague-Dawley rats were divided into normal control group and groups A, B, C, D according to the random number table, with 8 rats in each group. Rats in group A were loaded with 22.47 kPa pressure with a special pressure apparatus for 2.0 h in the region over gracilis, and then unloaded for 0.5 h. Rats in group B were treated with the same manoeuvre as that in group A for 3 times in one day. Rats in groups C and D were treated with the same manoeuvre as that in group B for 2 and 3 days. Rats in normal control group were free from pressure loading. Rats in groups A, B, C, and D were sacrificed after pressure loading, and then the central part of pressure loaded muscular tissues were harvested for observation of histomorphological change with HE staining; apoptotic nucleoli per millimeter pressure loaded muscular tissue were counted with Hoechst 33258 staining; the levels of binding protein (BIP), protein disulfide isomerase (PDI), C/EBP homologous protein (CHOP), and caspase-12 were assessed with Western blotting (denoted as gray level ratio of target protein to GAPDH). The same parts of gracilis of rats in normal control group were harvested for determination of all the indexes as above. Data were processed with one-way analysis of variance, LSD-t test was applied for paired comparison. RESULTS: (1) Histomorphological observation. Some pathological changes, including inflammatory cell infiltration, myofibers lysis, and vacuolar degeneration, etc. were observed in pressure loaded muscular tissue of rats in groups A, B, C, and D, but not in the same parts of gracilis muscle of rats in normal control group. Compared with those in normal control group [(2.7 ± 1.4) per millimeter muscular tissue], the number of apoptotic nuclei was significantly increased in pressure loaded muscular tissue of rats in groups A, B, C, and D [(14.5 ± 4.4), (11.0 ± 2.9) , (13.8 ± 5.1), (21.3 ± 6.0) per millimeter pressure loaded muscular tissue, with t values from 4.223 to 6.000, P values all below 0.01). (2) Western blotting. The protein expressions of BIP and PDI in rats of normal control group and groups A, B, C, D were respectively 0.64 ± 0.12, 1.20 ± 0.34, 1.59 ± 0.24, 1.17 ± 0.28, 1.44 ± 0.33; 0.48 ± 0.15, 0.61 ± 0.19, 1.23 ± 0.38, 0.37 ± 0.19, 0.29 ± 0.15, and they showed significant statistical difference (with F values respectively 5.32, 7.95, P < 0.05 or P < 0.01). The protein expressions of CHOP and caspase-12 in rats of normal control group and groups A, B, C, D were respectively 0.58 ± 0.18, 1.48 ± 0.27, 1.03 ± 0.21, 0.95 ± 0.30, 1.69 ± 0.34; 0.55 ± 0.12, 1.08 ± 0.31, 0.69 ± 0.24, 1.79 ± 0.20, 2.06 ± 0.47, with significant statistical difference (with F values respectively 8.17, 15.48, P values all below 0.01). CONCLUSIONS: ERS related proteins and their apoptotic pathway may play an important role in the formation of deep tissue injury of pressure ulcer in rats.

[Expressions of tumor necrosis factor-alpha and NF-kappa B in skeletal muscles and its effect on apoptosis in deep tissue injury of rats].

OBJECTIVE: To evaluate the changes of tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB) expression in muscle of pressure ulcer rats and explore the relationship with apoptosis. METHODS: Fifty-four male SD rats were randomly divided into nine groups (n = 6), the experiment groups were pressed 9 circles (3 circles/day, 3 days), then observed on the 1st, 3rd, hematoxylin and eosin staining under the microscope; the expression of TNF-alpha was detected by Western blot; the expressions of NF-kappaB and caspase-3 were determined by immunohistochemistry, and evaluated the relationship of TNF-alpha with NF-kappaB and caspase-3; the number of apoptotic cells in compressed muscle tissue was detected by Hoechst 33258 staining under the fluorescence microscope. RESULTS: Compared with the control group, histology examination showed that the tissue structure in experiment groups was in disorder, inter-space was wider, cell edema and the number of inflammatory cells were increased, the tissue was arranged in order and inflammatory cell recruitment was gradually attenuated. The expressions of TNF-alpha, NF-kappaB and caspase-3 were higher in the experiment groups than those in the control group (P < 0.05), reached their peak on the first day, gradually decreased on the 3nd day, but still had a significantly higher level than that in the control group (P < 0.01) on the 7th day; The number of apoptotic cells of experiment groups had a downward trend after the first rise under the fluorescence microscope; the expressions of TNF-alpha and NF-kappaB caspase-3 were found to have positive correlationship (P < 0.05), the expressions of NF-kappaB and caspase-3 were found to have positive correlationship (P < 0.01). CONCLUSION: Apoptosis is closely correlated with inflammation in deep tissue injury of pressure ulcer, NF-kappaB plays a role not only in the formation of inflammation, but also triggering apoptosis, which may induce the pathological change and clinical progress of pressure ulcer.

[Expressions of vascular endothelial growth factor and basic fibroblast growth factor in the late stage of pressure ulcer].

OBJECTIVE: To study the distribution and expressions of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in the III-IV stage of pressure ulcer wound, and to explore their correlation with ulceration. METHODS: Forty-one patients hospitalized in the two Affiliated Hospital of Wenzhou Medical College from June 2010 to March 2012 were recruited, including twenty-one patients with 23 pressure ulcer of stage III-IV, 14 acute injury patients, and 6 donors of normal skin. Samples harvested from the 41 patients through surgery were divided into four groups, including pressure ulcer centre group (n = 23), pressure ulcer margin group (n = 23), acute wound group (n = 14), and normal skin group (n = 6). The histological changes in wounds were observed after HE staining. The distribution of collagen fiber in wound was observed with Masson staining. Expressions of VEGF and bFGF in wounds were detected with immunohistochemical staining. Data were processed with independent samples t test and paired samples t test. RESULTS: (1) In the two pressure ulcer groups, large number of inflammatory cells were found in aggregation; the expression of collagen fiber was decreased or disappeared; the positive expressions of VEGF and bFGF were mainly located in fibroblasts and endothelial cells. The expression levels of VEGF and bFGF were respectively 100 ± 39, 132 ± 46 in pressure ulcer centre group, and 228 ± 48, 299 ± 80 in pressure ulcer margin group. The differences between the two pressure ulcer groups were statistically significant (with t values respectively 13.497 and 13.020, P values below 0.01). (2) In acute wound group, a large number of fibroblasts but a small amount of collagen fibers were observed; the positive expressions of VEGF and bFGF were mainly located in fibroblasts, with respective expression levels of 292 ± 59 and 443 ± 194, which were significantly higher than those of the two pressure ulcer groups (with t values from 2.370 to 11.570, P < 0.05 or P < 0.01). (3) In normal skin group, structure of tissue was appropriate, and abundant collagen fibers were observed; the expression levels of VEGF and bFGF were respectively 45 ± 18 and 54 ± 22, which were significantly lower than those of the other three groups (with t values from 3.983 to 14.087, P values all below 0.01). CONCLUSIONS: In contrast with those of the acute wounds, the expression levels of VEGF and bFGF are significantly decreased in the pressure ulcer wound at stage III-IV. It may be closely correlated with the decrease or cessation of the synthesis of collagen fiber.

Study of the mechanisms of acupuncture and moxibustion treatment for ulcerative colitis rats in view of the gene expression of cytokines.

AIM:To observe the effect of acupuncture and moxibustion on the expression of IL-1beta and IL-6 mRNA in ulcerative colitis rats.METHODS:The SD rat ulcerative colitis model was created by immunological method associated with local stimulation. Colonic mucosa was prepared from human fresh surgical colonic specimens, homogenized by adding appropriate amount of normal saline and centrifuged at 3000r/min. The supernatant was collected for measurement of protein conentration and then mixed with Freund adjuvant. This antigen fluid was first injected into the plantae of the model group rats, and then into their plantae, dorsa, inguina and abdominal cavities (noFreund adjuvant for the last injection) again on the 10th, 17th, 24th and 31st day. When a certain titer of serum anti colonic antibody was reached, 2% formalin and antigen fluid (no Freund adjuvant) were administered separately by enema. The ulcerative colitis rat model was thus set up. The animals were randomly divided into four groups: model control group (MC, n = 8), electro acupuncture group (EA, n = 8), herbs partition moxibustion group (HPM 8), normal control group (NC,n = 8). HPM: Moxa cones made of refined mugwort floss were placed on the medicinal pad (medicinal pad dispensing: Radix Aconiti praeparata, cortex Cinnamomi, etc) for Qihai (RN 6) and Tianshu (ST 25, bilateral) and ignited. Two moxa cones were used for each acupoint once a day and 14 times in all. EA: Tianshu (bilateral) and Qihai were stimulated by the intermittent pulse with 2Hz frequency, 4mA intensity for 20 minutes once a day and 14 times in all. After treatment, rats of all four groups were killed simultaneously. The spleen was separated and the distal colon was dissected. Total tissue RNA was isolated by the guanidinium thiocyanate phenol chloroform extraction method. RT-PCR technique was used to study the expression of IL-1 beta and IL-6 mRNA.RESULTS:IL-1 beta and IL-6 mRNAs were not detected in the spleen and colonic mucosa of the NC rats, whereas they were significantly expressed in that of the MC rats.IL-1 beta and IL-6 mRNAs were markedly lower in the EA and HPM rats than that in MC rats. There was no significant difference between the levels of IL-1 beta and IL-6 mRNAs in the EA and HPM rats. The expressions of IL-1 beta and IL-6 mRNAs were nearly the same in the spleen and colon of all groups.CONCLUSION:Acupuncture and moxibustion greatly inhibited the expression of IL-1 beta and IL-6 mRNA in the experimental ulcerative colitis rats.