[Intervention effect of Dachengqi Granule on apoptosis of small intestine smooth muscle cells in rats with multiple organ dysfunction syndrome].

OBJECTIVE: To observe the intervention of Dachengqi Granule (DG) on the apoptosis of small intestine smooth muscle cells (SMCs) in rats with multiple organ dysfunction syndrome (MODS) and its mechanisms. METHODS: Healthy 100 adult Wistar rats were randomly divided into the control group (n =20), the MODS model group (n =40), and the DG group (n =40).E. coli suspension was peritoneally injected to rats in the model group and the DG group to establish bacterial peritonitis induced MODS model. DG at 1 mL/100 g was administered by gastrogavage to rats of the DG group, twice daily for 3 successive days. Twenty-four hours after modeling, the proximal segment of intestine was taken and stained by using terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) and immunohistochemistry. Changes of apoptosis quantity of SMCs and the expression of Bcl-2 associated X protein (Bax), B cell lymphoma/leukemia-2 (Bcl-2) and cytochrome c protein (Cyt c) in mitochondrial apoptotic signaling pathway were observed. RESULTS: Compared with the control group, the apoptosis quantity of SMCs and the expression of Bax and Cyt c protein significantly increased, and the expression of Bcl-2 protein significantly decreased in the MODS model group (P <0.01). Compared with the MODS model group, the apoptosis quantity of SMCs and the expression of Bax and Cyt c proteins significantly decreased, and the expression of Bcl-2 protein significantly increased in the DG group (allP <0.01). CONCLUSION: DG could inhibit apoptosis of SMCs through suppressing activation of mitochondrial apoptotic signaling pathway in intestinal SMCs, thus promoting the recovery of the gastrointestinal motility function in rats with MODS.

[Repair of xiangsha liujunzi decoction on damage of interstitial cells of cajal and gap junction in the gastric muscular layer of rats of Pi-Qi deficiency syndrome: an experiment study].

OBJECTIVE: To explore the repair of Xiangsha Liujunzi Decoction (XSLJZD) on interstitial cells of Cajal (ICC) and gap junction (GJ) in the gastric muscular layer of rats of Pi-qi deficiency syn- drome (PQDS). METHODS: PQDS was established using purgative method with bitter and cold drugs in 30 healthy Wistar rats. After successful modeling they were randomly divided into the treatment group and the model group, 15 in each group. Another 15 healthy Wistar rats were recruited as the healthy control group. Rats in the treatment group were gastric administered with XSLJZD at 2 mL/100 g body weight, once daily for 14 successive days. Equal volume of normal saline was gastrically administered to those in the healthy control group and the model group. The gastric muscle tissues were taken out before modeling, before intervention, and after intervention, respectively. Ultrastructural changes of ICC and GJ were observed using transmission electron microscope (TEM). The number and distribution of Connexin43 (Cx43) were detected using immunohistochemistry. RESULTS: Results of TEM indicated that compared with the healthy control group, both ICC and GJ in the model group showed obvious injury. ICC and GJ were apparently repaired after intervention in the treatment group. Compared with the same group before modeling, the integrated optical density (IOD) of the Cx43 expression significantly decreased in the model group before and after intervention (P <0.05). Compared with before intervention, the IOD of the Cx43 expression significantly increased in the treatment group (P <0.05). Compared with the healthy control group, the IOD of the Cx43 expression significantly decreased in the model group before and after intervention (P <0.05). Compared with the model group, the IOD of the Cx43 expression significantly increased in the treatment group (P <0.05). CONCLUSIONS: Ultrastructures of ICC and GJ in the gastric muscular layer of rats of PQDS were obviously damaged. XSLJZD could repair the structural damage of ICC and GJ in the gastric muscle tissues of rats of PQDS.

Clinical and molecular analysis of hereditary non-polyposis colorectal cancer in Chinese colorectal cancer patients.

AIM: To analyze the frequency of hereditary non-polyposis colorectal cancer (HNPCC) in Chinese colorectal cancer (CRC) patients, and to discuss the value of microsatellite instability (MSI) and/or immunohistochemistry (IHC) for MSH2/MLH1 protein analysis as pre-screening tests in China. METHODS: The Amsterdam criteria I and II (clinical diagnosis) and/or germline hMLH1/hMSH2 mutations (genetic diagnosis) were used to classify HNPCC families. Genetic tests, including microsatellite instability, immunohistochemistry for MSH2/MLH1 proteins and hMSH2/hMLH1 genes, were performed in each proband. RESULTS: From July 2000 to June 2004, 1988 patients with colorectal cancer were analysed and 114 CRC patients (5.7%) from 48 families were categorized as having HNPCC, including 76 from 26 families diagnosed clinically and 38 from the other 22 families diagnosed genetically. The sensitivity and specificity of high MSI and IHC for predicting mutations were 100% and 54%, and 79% and 77%, respectively. CONCLUSION: The frequency of HNPCC is approximately 10% among all Chinese CRC cases. The MSI and IHC detections for hMSH2/hMLH1 proteins are reliable pre-screening tests for hMLH1/hMSH2 germline mutations in families suspected of having HNPCC.

[Role of polymorphonuclear neutrophil apoptosis and expression of Fas and caspase-3 in the systemic inflammatory response syndrome].

OBJECTIVE: To study the role of the polymorphonuclear neutrophil (PMN) apoptosis and expression of Fas and caspase-3 in the systemic inflammatory response syndrome (SIRS). METHODS: Eight acute pancreatitis patients with SIRS, 6 healthy control subjects were enrolled to study apoptosis of PMN in peripheral blood samples, expression of Fas/Fas ligand (FasL) and caspase-3 in the PMN, the levels of serum interleukin-6 (IL-6) and IL-8 were observed. RESULTS: Spontaneous apoptosis was significantly delayed in PMN from the SIRS patients with higher serum IL-6 and IL-8 levels compared with controls (both P<0.01). PMN apoptosis rate in peripheral blood of patients with SIRS was lowered than that of controls (P<0.01). The expressions of Fas and caspase-3 in the peripheral circulating PMN were higher in the controls than those in the SIRS patients (both P<0.01). Serum FasL expression was not found by Western blotting 24 hours after culture of PMN in vitro. CONCLUSION: Peripheral circulating PMN from acute pancreatitis patients with SIRS show delayed apoptosis, decreased expressions of Fas and caspase-3, and prolonged PMN survival may contribute to the development of systemic inflammatory injury characteristic of SIRS.

Endovascular stenting of spontaneous isolated dissection of the superior mesenteric artery: A case report and literature review.

RATIONALE: Spontaneous isolated dissection of the superior mesenteric artery (SID-SMA) is a rare arterial disease that is difficult to differentiate from other diseases because of lack of specific clinical manifestation and for which there is no available optimal management strategy. PATIENT CONCERNS: A 58-year-old male patient visited our emergency room with sudden onset of moderate-severe epigastric abdominal pain of uncertain cause. DIAGNOSES: Computed tomography scanning showed a characteristic "double lumen sign" of the superior mesenteric artery, and further computed tomography angiography findings revealed a dissected segment of the superior mesenteric artery. INTERVENTIONS: Conservative management was administered for 5 days, but the abdominal pain remained. Subsequently, an endovascular stent was placed in the affected superior mesenteric artery. Postoperative antiplatelet therapy was administered for 6 months. OUTCOMES: The abdominal pain was relieved. Six months later, a follow-up of computed tomography angiography showed that the stent placed had no interval narrowing. LESSONS: Based on our review and the illustration of this case, endovascular stenting may be a preferred rescue treatment in SID-SMA patients for whom initial conservative treatment fails.

Roles of PD-1, Tim-3 and CTLA-4 in immunoregulation in regulatory T cells among patients with sepsis.

OBJECTIVE: This study aims to elucidate the roles of PD-1, Tim-3 and CTLA-4 in sepsis. METHODS: Sepsis patients (n = 182) were selected as sepsis group and divided into three subgroups: mild sepsis group, severe sepsis group and septic shock group; 185 healthy volunteers were enrolled as control group. Flow cytometry and blood routine examination were performed for T lymphocytes and surface co-stimulatory molecules expressions. Pearson correlation test was applied for the correlation of co-stimulatory molecules expressions on T lymphocytes with critical illness in sepsis. Logistic regression analysis was conducted for risk factors in sepsis. RESULTS: Heart rate and WBC in subgroups were higher than control group (P < 0.05). The differences in APACHE II, SAP II and SOFA score among subgroups were statistically significant (P < 0.05). Compared with control group, lymphocyte ratio and percentage of CD4(+) T cells reduced in subgroups (P < 0.05). The differences in expression levels of CD4(+)PD-1(+), CD8(+)PD-1(+), and CD8(+)CTLA-4(+) showed statistical significances (P < 0.05). Apparently, expression levels of CD4(+)TIM-3(+), CD8(+)TIM-3(+), CD4(+)PD-1(+), CD8(+)PD-1(+), and CD4(+)CTLA-4(+) were positively correlated with APACHE II score (all P < 0.05). Logistic regression analysis showed that heart rate and expression level of CD4(+)PD-1(+) might be risk factors while the percentage of CD4(+) T cells might be a protective factor for sepsis (P < 0.05). CONCLUSION: PD-1 aggravates immune responses consistent with promotion of T cell exhaustion in sepsis. Expression level of CD4(+)PD-1(+) and heart rate are potential risk factors while percentage of CD4(+) T cells is a possible protective factor for sepsis.

Interventional effects of da-cheng-qi decoction on enteric nerve system in a rat model of multiple organ dysfunction syndrome.

In this study, we investigate the morphologic changes of enteric nerve system (ENS) and the expression of neurotransmitters, acetylcholine (ACh), substance P (SP), vasoactive intestinal peptide (VIP) and nitric oxide synthase (NOS), in small bowel of rats undergoing multiple organ dysfunction syndrome (MODS). Undergoing MODS, fluorescence integral optical density (IOD) value of enteric nerve fibers were significantly decreased (P<0.05), and the network structure of ENS was destroyed. The expression of ACh, SP, VIP and NOS was inhibited, IOD value of the four neurotransmitters was significantly decreased (P<0.05). After intervention of DCQD, the fluorescence IOD value of enteric nerves were significantly increased (P<0.05), and the network structure of ENS was repaired. The expression of ACh, SP, VIP and NOS was recovered, fluorescence IOD value of the four neurotransmitters was significantly increased (P<0.05). In conclusion, the gastrointestinal motility disorders undergoing MODS may be closely related to the morphology destroy of ENS and down regulation of neurotransmitters (ACh, SP, VIP and NOS) expression. DCQD could promote gastrointestinal motility through protecting the morphology of ENS and up regulation of neurotransmitters (ACh, SP, VIP and NOS) expression.

Effects of Dachengqi Decoction () on morphological changes in enteric nerve system of rats with multiple organ dysfunction syndrome.

OBJECTIVE: To observe the morphological changes in enteric nerve system (ENS) of rats with multiple organ dysfunction syndrome (MODS) treated by Dachengqi Decoction (, DCQD). METHODS: Fifty Wistar rats were randomly assigned to the control group, MODS model group and DCQD treated group. The rats in MODS model group and DCQD treated group were injected Escherichia coli (E. coli) suspension into abdominal cavity under sterile condition. The DCQD treated group was gavaged with DCQD 2 days before the E. coli suspension was injected. Twenty-four hours after injection, the proximal segment of intestine was resected and studied by immunohistofluorescence using vesicular acetylcholine transporter, vasoactive intestinal polypeptide (VIP), substance P (SP) and neuronal nitric oxide synthase (nNOS) antibodies. The whole-mount preparations were observed by laser scanning confocal microscope to detect the changes of quantity and fluorescence integral optical density (IOD) value of intestine enteric nerves. RESULTS: Compared with the control group, the quantity and IOD value of acetylcholine (ACh), VIP, SP and nitric oxide (NO) nerves of intestine in the MODS group were significantly decreased (P<0.01), and the network of enteric nerves was remarkably disrupted. Compared with the MODS group, the quantity and fluorescence IOD value of ACh, VIP, SP and NO nerves in the DCQD group were significantly increased (P<0.01), and the network of enteric nerves was remarkably recovered. CONCLUSION: DCQD can protect and repair damage in the network of ACh, SP, NO and VIP nerves in rats with MODS, which may be one of mechanisms involved in promoting gastrointestinal motility by DCQD.

Relationship of serum mannose-binding lectin levels with the development of sepsis: a meta-analysis.

Many studies have evaluated the association between serum levels of mannose-binding lectin (MBL) and sepsis; however, the findings are inconclusive and conflicting. For a better understanding of MBL in sepsis, we conducted a comprehensive meta-analysis. Potential relevant studies were identified covering Science Citation Index, the Cochrane Library, PubMed, Embase, CINAHL, and Current Contents Index databases. Two reviewers extracted data and assessed studies independently. Statistical analyses were conducted with the version 12.0 STATA statistical software. Ten papers were collected for meta-analysis. Results identified that sepsis patients had considerably lower MBL level than those in the controls (standardized mean difference (SMD) = 1.59, 95 % confidence interval (95%CI) = 0.86∼2.31, P < 0.001). Ethnicity-subgroup analysis showed that sepsis patients were associated with decreased serum MBL level in contrast to the healthy controls in Asians (SMD = 3.07, 95%CI = 1.27∼4.88, P = 0.001) and Caucasians (SMD = 1.00, 95%CI = 0.35∼1.65, P = 0.003). In the group-stratified subgroup analysis, subjects with lower serum MBL level did underpin susceptibility to sepsis in the infants subgroup (SMD = 2.57, 95%CI = 1.59∼3.55, P < 0.001); however, this was not the case in the adults subgroup (SMD = 0.13, 95%CI = -1.30∼1.55, P = 0.862). Our study suggests an important involvement of serum MBL level in sepsis patients considering their lower level compared to controls, especially among infants.

Serum S100B level may be correlated with carbon monoxide poisoning.

OBJECTIVE: To investigate the correlation between serum S100B level and carbon monoxide (CO) poisoning by meta-analysis. METHODS: By searching both English and Chinese language-based electronic databases (PubMed, EBSCO, Ovid, Springerlink, Wiley, Web of Science, Wanfang databases, China national knowledge infrastructure (CNKI), VIP database, etc.) thoroughly, we tabulated and analyzed the collected data with the use of Comprehensive Meta-analysis 2.0 (CMA 2.0). RESULTS: Totally 108 studies have been searched initially (92 studies in Chinese, 16 studies in English). Nine case-control studies (4 studies in English, 5 in Chinese) were chosen for an updated meta-analysis including 542 patients with CO poising and 236 healthy controls. Results identified that the serum S100B level were obviously higher than that in healthy controls (SMD=1.600, 95% CI=1.055-2.145, P<0.001). A subgroup based on the ethnicities revealed that the serum S100B level in Caucasian and Asian subgroups was clearly higher than serum S100B level in healthy controls (Asians: SMD=2.0624, 95% CI=1.736-3.511, P<0.001; Caucasians: SMD=0.447, 95% CI=0.197-0.697, P<0.001). CONCLUSION: Serum S100B level may be correlated with the CO poisoning and could be effective biomarker for early diagnosis and treatment monitoring in CO poisoning.

Prospective study of biofeedback retraining in patients with chronic idiopathic functional constipation.

AIM: To determine the efficacy and long-term outcome of biofeedback treatment for chronic idiopathic constipation and to compare the efficacy of two modes of biofeedback (EMG-based and manometry-based biofeedback). METHODS: Fifty consecutive contactable patients included 8 cases of slow transit constipation, 36 cases of anorectic outlet obstruction and 6 cases of mixed constipation. Two modes of biofeedback were used for these 50 patients, 30 of whom had EMG-based biofeedback, and 20 had manometry-based biofeedback. Before treatment, a consultation and physical examination were done for all the patients, related information such as bowel function and gut transit time was documented, psychological test (symptom checklist 90, SCL90) and anorectic physiological test and defecography were applied. After biofeedback management, all the patients were followed up. The Student's t-test, chi-squared test and Logistic regression were used for statistical analysis. RESULTS: The period of following up ranged from 12 to 24 months (Median 18 months). 70 % of patients felt that biofeedback was helpful, and 62.5 % of patients with constipation were improved. Clinical manifestations including straining, abdominal pain, bloating, were relieved, and less oral laxative was used. Spontaneous bowel frequency and psychological state were improved significantly after treatment. Patients with slow and normal transit, and those with and without paradoxical contraction of the anal sphincter on straining, benefited equally from the treatment. The psychological status rather than anorectal test could predict outcome. The efficacy of the two modes of biofeedback was similar without side effects. CONCLUSION: This study suggests that biofeedback has a long-term effect with no side effects, for the majority of patients with chronic idiopathic constipation unresponsive to traditional treatment. Pelvic floor abnormalities and transit time should not be the selection criteria for treatment.

Etiology and management of hemmorrhage in spontaneous liver rupture: a report of 70 cases.

AIM: To analyze the causes and management of hemorrhage in spontaneous liver rupture. METHODS: Seventy cases of spontaneous liver rupture were retrospectively analyzed for causes of hemorrhage and therapeutic effects of surgical approaches. RESULTS: It was demonstrated that the causes of spontaneous liver rupture were primary liver cancer in 60 cases (85.7 %), cirrhosis in 3 cases (4.3 %), liver angioma in 2 cases (2.9 %), liver adenoma in 4 cases (5.7 %),and secondary liver cancer in 1 case (1.4 %). Hemostasis was achieved with surgical approaches in 68 cases (97.1 %) and non-surgical approaches in 2 cases (2.9 %). Surgical interventions included suture, ligation of hepatic artery, hepatic artery chemoembolization and partial hepatic resection. CONCLUSION: The results suggest that surgical intervention is still the main therapeutic method and the best procedure that should be selected according to causes of disease and patient's condition and history.

Signal pathways involved in emodin-induced contraction of smooth muscle cells from rat colon.

AIM: To investigate the effects induced by emodin on single smooth muscle cells from rat colon in vitro, and to determine the signal pathways involved. METHODS: Cells were isolated from the muscle layers of Wistar rat colon by enzymatic digestion. Cell length was measured by computerized image micrometry. Intracellular Ca2+ ([Ca2+]i) signals were studied using the fluorescent Ca2+ indicator fluo-3 and confocal microscopy. PKCalpha distribution at rest state or after stimulation was measured with immunofluorescence confocal microscopy. RESULTS: (1) Emodin dose-dependently caused colonic smooth muscle cells contraction; (2) emodin induced an increase in intracellular Ca2+ concentration; (3) the contractile responses induced by emodin were respectively inhibited by preincubation of the cells with ML-7 (an inhibitor of MLCK) and calphostin C (an inhibitor of PKC); (4) Incubation of cells with emodin caused translocation of PKCalpha from cytosolic area to the membrane. CONCLUSION: Emodin has a direct contractile effect on colonic smooth muscle cell. This signal cascade induced by emodin is initiated by increased [Ca2+]i and PKCalpha translocation, which in turn lead to the activation of MLCK and the suppression of MLCP. Both of them contribute to the emodin-induced contraction.

Effect of arsenic trioxide on rat hepatocellular carcinoma and its renal cytotoxity.

AIM: To study the effect of arsenic trioxide (As(2)O(3)) on rat experimental hepatocellular carcinoma and its renal cytotoxicity. METHODS: The hepatocellular carcinoma model was established by diethaylnitrosamine perfusion in stomach of 120 Wistar rats, and the treatment began at the end of 20 weeks. Before the treatment, the rat models were randomly divided into 5 groups. In the treatment groups, three doses of As(2)O(3) were injected into rat abdominal cavity; the total time of drug administration was 4 weeks. Cisplatin control or the blank group was injected into abdominal cavity with equal amount of cisplatin or saline at the same time, respectively. On the 7th, 14th and 28th day after the treatment, the hepatocellular carcinoma nodules were obtained and the morphologic changes of hepatocellular carcinoma cells were observed under light and electron microscopes; Immunohistochemistry (S-P methods) was employed to detect the expression of bcl-2, bax and PCNA in hepatocellular carcinoma tissues; flow cytometry (TUNEL assay) was used to detect the apoptosis of liver cancer cells and the change of cytokinetics. On the 28th day, the renal was obtained and its histologic change was observed under light microscope, and immunohistochemistry (SP stain) was also employed to detect the expression of bcl-2 and PCNA. Cisplatin and saline solution were used as the control. RESULTS: As(2)O(3) could induce the apoptosis of rat liver cancer cells and exhibited typical morphologic changes. The incidence of apoptosis of hapatocellular carcinoma cells was elevated (P=0.001). The elevation was higher in the group of middle-dose of As(2)O(3) (1 mg/kg(-1)) significantly than the other arsenic groups and the controls (P=0.001). Large dose of As(2)O(3) (5 mg/kg(-1)) was able to arise the incidence of apoptosis, but also produced a large amount of necrosis and inflammatory reaction. Middle dose of As(2)O(3) dramatically increased the cell number in G2/M phase (P=0.0001), and apoptosis happened apparently. The expression of bcl-2 and bax was related to the dose of As(2)O(3). With the up-regulation of apoptotic incidence, the ratio of bcl-2/bak decreased. But the incidence of apoptosis was not the highest status and the ratio of bcl-2/bax was at the lowest when the highest-dose of As(2)O(3) was used. There was significant difference among the PCNA indexes (PCNA LI) of the five groups. Of them, three arsenic groups all showed decrease of different degrees, and this down-regulation was most obvious in group A. There was significant difference among the three groups (P=0.016). Under the light microscope, the rat kidney in the cisplatin group exhibited tubular epithelium swelling and degeneration, protein casts in collecting tubules; While all arsenic groups didn't show the significant changes (P=0.013). In the arsenic groups, the expression of bcl-2 in the renal tubular epithelium was increased (P=0.005), no obvious changes happened to PCNA LI. But in the group of cisplatin, the PCNA LI increased significantly (P=0.001). CONCLUSION: As(2)O(3) can induce apoptosis of rat hepatocellular carcinoma cells. And there is optimum dose; too high dose will induce the cytotoxic effect, while certain dose of As(2)O(3) is able to block the cell cycle at G2/M phase. As(2)O(3) had the most remarkable influence on G2/M cells, and it can also induce apoptosis to cells at other phases. As(2)O(3) can restrain the proliferation of rat hepatocellular carcinoma cells, in a dose-time dependent manner; Compared with cisplatin, As(2)O(3) didn't show obvious renal toxicity, which was related to the increasing expression of bcl-2 in renal tubular epithelium, the inhibition of apoptosis and the anti-oxidation effects.

Contractile effects and intracellular Ca2+ signalling induced by emodin in circular smooth muscle cells of rat colon.

AIM: To investigate whether emodin has any effects on circular smooth muscle cells of rat colon and to examine the mechanism underlying its effect. METHODS: Smooth muscle cells were isolated from the circular muscle layer of Wistar rat colon and the cell length was measured by computerized image micrometry. Intracellular Ca(2+) ([Ca(2+)]i) signalling was studied in smooth muscle cells using Ca(2+) indicator Fluo-3 AM on a laser-scanning confocal microscope. RESULTS: Emodin dose-dependently induced smooth muscle cells contraction. The contractile responses induced by emodin were inhibited by preincubation of the cells with ML-7 (an inhibitor of MLCK). Emodin caused a large, transient increase in [Ca(2+)]i followed by a sustained elevation in [Ca(2+)]i. The emodin -induced increase in [Ca(2+)]i was unaffected by nifedipine, a voltage-gated Ca(2+)-channel antagonist, and the sustained phase of the rising of [Ca(2+)]i was attenuated by extracellular Ca(2+) removal with EGTA solution. Inhibiting Ca(2+) release from ryanodine-sensitive intracellular stores by ryanodine reduced the peak increase in [Ca(2+)]i. Using heparin, an antagonist of IP(3)R, almost abolished the peak increase in [Ca(2+)]i. CONCLUSION: Emodin has a direct excitatory effect on circular smooth muscle cells in rat colon mediated via Ca(2+)/CaM dependent pathways. Furthermore, emodin-induced peak [Ca(2+)]i increase may be attributable to the Ca(2+) release from IP(3) sensitive stores, which further promote Ca(2+) release from ryanodine-sensitive stores through CICR mechanism. Additionally, Ca(2+) influx from extracellular medium contributes to the sustained increase in [Ca(2+)]i.

[Effect of dachengqi granule on human gastrointestinal motility].

OBJECTIVE: To study the therapeutic effect and mechanism of Dachengqi granule (DCQG) on some digestive motility disturbed diseases. METHODS: Gastroduodenojejunal manometry, electrogastrography (EGG), RIA of motilin and orocecal transit time test were applied to directly observe the effect of DCQG on human gastrointestinal motility. RESULTS: DCQG could significantly improve the postoperational EGG disorder, elevate the amplitude and time of migrating motor complex (MMC) phase III, prevent gastrointestinal reversed peristalsis, increase the blood level of motilin, decrease the orocecal transit time, and promote the recovery of gastrointestinal motility. CONCLUSION: DCQG is an effective digestive kinetic agent, which could be medicated conveniently in treating digestive motility disturbed diseases.

[Effect of emodin on motility signal transduction in colonic smooth muscle cells in rats with multiple organ dysfunction syndrome].

OBJECTIVE: To observe the effect of emodin on motility signal transduction and calcium ion in colonic smooth muscle cells (SMC) in rats with bacterial peritonitis caused multiple organ dysfunction syndrome (MODS). METHODS: Observation was conducted in colon of MODS model rats on (1) effects of emodin on the contraction of muscular strip and cells of colonic smooth muscle, and influences of specific myoglobulin light chain kinase inhibitor (ML-7) and selective proteinkinase C inhibitor (Calphostin C) on these effects; and (2) effect of emodin on calcium ion in SMC. RESULTS: Emodin could directly contract the muscular strip and cells of smooth muscle; ML-7 and Calphostine could inhibit these contractile action to some extent. Under MODS condition, emodin could still increase the intracellular calcium ion concentration; this effect could be inhibited by heparin (inosamine triphosphate receptor inhibitor IP3 and ryanodine receptor inhibitor in MODS model but the calcium chelator EGTA and nifedipine (the specific cell membrane voltage dependent calcium channel blocker) showed no influence on it. CONCLUSION: Emodin could directly contract the colonic smooth muscle in MODS model rats, which is mediated by raise the signal path MLCK of calcium ion and the PKCa path for increase calcium sensibility. The mechanism of increasing calcium ion is mainly through IP3 and RyR the two calcium ion channel receptor in the sarcoplasm.

Effect of da-cheng-qi decoction on the repair of the injured enteric nerve-interstitial cells of cajal-smooth muscle cells network in multiple organ dysfunction syndrome.

Wistar rats were randomly divided into control group, multiple organ dysfunction syndrome (MODS) group, and Da-Cheng-Qi decoction (DCQD) group. The network of enteric nerves-interstitial cells of Cajal- (ICC-) smooth muscle cells (SMC) in small intestine was observed using confocal laser scanning microscopy and transmission electron microscopy. The results showed that the numbers of cholinergic/nitriergic nerves, and the deep muscular plexus of ICC (ICC-DMP) and connexin43 (Cx43) in small intestine with MODS were significantly decreased. The network integrity of enteric nerves-ICC-SMC was disrupted. The ultrastructures of ICC-DMP, enteric nerves, and SMC were severely damaged. After treatment with DCQD, the damages were repaired and the network integrity of enteric nerves ICC-SMC was significantly recovered. In conclusion, the pathogenesis of gastrointestinal motility dysfunction in MODS in part may be due to the damages to enteric nerves-ICC-SMC network and gap junctions. The therapeutic mechanism of DCQD in part may be that it could repair the damages and maintain the integrity of enteric nerves ICC-SMC network.

Morphological changes in network of enteric nerve-interstitial cells of Cajal-smooth muscle cells in rats with multiple organ dysfunction syndrome and therapeutic effects of Dachengqi decoction (大承气汤).

OBJECTIVE: To observe the effects of Dachengqi Decoction (大承气汤, DCQD) on morphological changes in the network of enteric nerve-interstitial cells of Cajal (ICCs)-smooth muscle cells (SMC) of enteric deep muscular plexuses (DMP) in the rats with multiple organ dysfunction syndrome (MODS). METHODS: One hundred Wistar rats of both sexes weighing 200 to 250 g were randomly divided into the control group, MODS group, and DCQD group. The morphologic changes of enteric nerve-ICC-SMC network in the DMP of intestine was observed using c-Kit and vesicular acetylcholine transporter/neuronal nitric oxide synthase immunohistochemical double-staining with whole-mount preparation technique, confocal laser scanning microscopy, and electron microscopy. RESULTS: Compared with the control group, the distribution and densities of cholinergic/nitrergic nerves and ICC in the DMP (ICC-DMP) of intestine in the MODS group were significantly decreased (P<0.01), and the network of cholinergic nerve-ICC-SMC was disrupted; and the ultrastructural features of ICC-DMP, enteric nerve, and SMC were severely damaged. After treatment with DCQD, the damage in the network of enteric nerve-ICC-SMC was significantly recovered. Compared with the MODS group, the distribution and densities of cholinergic/nitrergic nerves and ICC-DMP in the DCQD group were significantly increased (P<0.01); and the ultrastructural features of ICC-DMP, enteric nerve, smooth muscle cells were significantly recovered. CONCLUSIONS: DCQD can improve the gastrointestinal motility in MODS. The mechanism may be related to the effect of repairing the damages in the network of enteric nerve-ICC-SMC.

Effects of dendroaspis natriuretic peptide on calcium-activated potassium current and its mechanism.

In this study, we sought to investigate the effect of dendroaspis natriuretic peptide (DNP) on calcium-activated potassium current (I K(Ca)) and its mechanism in gastric antral circular smooth muscle cells (SMCs) using the whole-cell patch-clamp technique. DNP concentration-dependently increased macroscopic I K(Ca) and spontaneous transient outward currents (STOCs) in freshly isolated guinea pig gastric antral circular SMCs. The effects of DNP on I K(Ca) and/or STOCs were not blocked by applying calcium-free bath solution or the ryanodine receptor (RyR) antagonist ryanodine (10 microM), but they were inhibited by the inositol triphosphate receptor (IP3R) inhibitor heparin or the guanylate cyclase inhibitor LY83583. Moreover, a DNP-induced increase in STOCs was potentiated by the cyclic guanosine monophosphate (cGMP)-sensitive phosphoesterase inhibitor zaprinast. In conclusion, our results suggest that DNP increases I K(Ca) in gastric antral circular SMCs by increasing cGMP production and activating IP3Rs.