Notch-Targeted Therapeutic in Colorectal Cancer by Notch1 Attenuation Via Tumor Microenvironment-Responsive Cascade DNA Delivery.

The Notch signaling is a key molecular pathway that regulates cell fate and development. Aberrant Notch signaling can lead to carcinogenesis and progression of malignant tumors. However, current therapies targeting Notch pathway lack specificity and induce high toxicity. In this report, a tumor microenvironment-responsive and injectable hydrogel is designed to load plasmid DNA complexes as a cascade gene delivery system to achieve precise Notch-targeted gene therapy of colorectal cancer (CRC). The hydrogels are prepared through cross-linking between phenylboric acid groups containing poly(oligo(ethylene glycol)methacrylate) (POEGMA) and epigallocatechin gallate (EGCG), used to load the complexes between plasmid DNA encoding short hairpin RNAs of Notch1 (shNotch1) and fluorinated polyamidoamine (PAMAM-F) (PAMAM-F/shNotch1). In response to low pH and H2O2 in tumor microenvironment, the hydrogel can be dissociated and release the complexes for precise delivery of shNotch1 into tumor cells and inhibit Notch1 activity to suppress malignant biological behaviors of CRC. In the subcutaneous tumor model of CRC, PAMAM-F/shNotch1-loaded hydrogels can accurately attenuate Notch1 activity and significantly inhibit tumor growth without affecting Notch signal in adjacent normal tissues. Therefore, this therapeutic system can precisely inhibit Notch1 signal in CRC with high responsiveness and low toxicity, providing a promising Notch-targeted gene therapeutic for human malignancy.

Otitis media with effusion in preschool children with adenoid hypertrophy: Risk factors and nursing care.

AIM: To evaluate the influencing factors of otitis media with effusion (OME) in children with adenoid hypertrophy and to provide evidence for clinical treatment and care of children with adenoid hypertrophy. DESIGN: A retrospective study. METHODS: Preschool children with adenoid hypertrophy treated in our hospital from 1 January 2021 to 30 July 2022 were included. We analysed the characteristics of OME and non-OME children with adenoid hypertrophy. Pearson correlation analysis and logistic regression analysis were performed to evaluate the risk factors for OME in children with adenoid hypertrophy. CONCLUSION: A total of 166 children with adenoid hypertrophy were included; the incidence of OME in children with adenoid hypertrophy was 34.94%. The incidence of OME decreased significantly with the increase in age (p = 0.014). Logistic regression analysis showed that age < 3 years (OR = 3.149, 95%CI: 2.812-3.807) and duration of adenoid hypertrophy ≥12 months (OR = 2.326, 95%CI: 2.066-2.612) were the risk factors of OME in children with adenoid hypertrophy (all p < 0.05). PATIENT CONTRIBUTION: The incidence of adenoid hypertrophy with OME is high in preschool children, and it is related to the age and duration of adenoid hypertrophy.

[Response of Soil Fungal Community to Biochar Application Under Different Irrigation Water Salinity].

Saline water irrigation can alleviate the shortage of freshwater resources in the northwest arid zone, but long-term saline water irrigation can damage the soil fungal community structure. To alleviate the harm caused by salinity, biochar is used as a soil amendment to improve the soil fungal community structure. To investigate the intrinsic link between biochar application and the structural diversity of fungal communities in saline soils, two irrigation water salinity levels were set:0.35 dS·m-1 (fresh water) and 8.04 dS·m-1 (saline water). At each irrigation water salinity, two levels of biochar application were set:0 t·hm-2 (no application) and 3.7 t·hm-2 (application). High-throughput sequencing results showed that compared to that under fresh water irrigation, saline water irrigation increased fungal community species diversity and decreased fungal community species richness; biochar application under saline water irrigation reduced soil fungal community species diversity and species richness. The dominant fungal phyla in the soils of each treatment were Ascomycota, Mortierellomycota, Basidiomycota, Chytridiomycota, Glomeromycota, Rozellomycota, and Cysticercales, and the dominant genera were Gibberella, Chaetomium, Sarocladium, Stachybotrys, and Fusarium. Compared to that under freshwater irrigation, saline water irrigation significantly increased the relative abundance of Basidiomycota and Chytridiomycota and significantly decreased the relative abundance of Ascomycota and Rozellomycota. The application of biochar under saline irrigation significantly increased the relative abundance of Ascomycota and Sarocladium but significantly decreased the relative abundance of Basidiomycota, Chaetomium, and Fusarium. LEfSe analysis showed that under the condition of no biochar application, saline irrigation reduced the number of potential biomarkers of fungal communities, whereas the application of biochar under the condition of saline irrigation increased the number of potential biomarkers of fungal communities. These results indicated that the application of biochar can improve the saline soil environment and fungal community structure and provide a theoretical basis for reasonable brackish water irrigation and soil fertilization in arid areas.

Head and neck carcinoma in children: A clinicopathological study of 42 cases.

Background/purpose: Cancer is an important part of the global burden of childhood diseases. Head and neck carcinoma in children is rare and related research is limited. This study aimed to investigate the clinicopathological features of childhood head and neck carcinoma. Materials and methods: Forty-two cases of childhood head and neck carcinoma treated in our institution were reviewed and analyzed. Results: Median age overall was 11 years. Twenty-three patients (54.8%) were male and 19 (45.2%) were female. Parotid gland location was most common (54.8%). Mucoepidermoid carcinoma and squamous cell carcinoma were the most common histological types (57.1% and 11.9%, respectively). Two patients had a history of bone marrow transplantation and two had a history of odontogenic keratocyst. The recurrence rate after treatment was 8.6%. Conclusion: Early diagnosis and treatment and close follow-up of childhood head and neck carcinoma are warranted to prevent recurrence and improve clinical outcome.

Adenoid Ameloblastoma Shares Clinicopathologic, Immunohistochemical, and Molecular Features With Dentinogenic Ghost Cell Tumor: A Comparative Analysis.

The updated classification of odontogenic tumors by the World Health Organization (WHO) has included adenoid ameloblastoma (AA) as a distinct entity. However, distinguishing between AA and dentinogenic ghost cell tumor (DGCT) can still be challenging due to their significant morphologic similarities. In this study, we aimed to compare the clinicopathologic, immunohistochemical, and molecular characteristics of AA and DGCT to aid in their differentiation and to shed light on their pathologic mechanisms. Thirteen cases of AA and 14 cases of DGCT (15 samples) were analyzed, along with 11 cases of adenomatoid odontogenic tumor (AOT) and 18 cases of conventional ameloblastoma (AM) for comparative purposes. The study found that AA and DGCT shared a similar long-term prognosis. Immunohistochemically, all cytokeratins detected, except CK8/18, were not statistically significant in differentiating AA and DGCT, while there was a statistically significant difference in the immunophenotype of CK7 and CK10/13 between AA and AM. Nuclear ß-catenin accumulation were detected in all cases of AA and DGCT, while AOTs and AMs exhibited cytoplasmic ß-catenin. Molecularly, CTNNB1 hotspot mutations were found in only 1 case of AA (1/13), but not found in the other 3 types of tumors. BRAF p.V600E mutation was positive in 2/13 (15%) AA, 1/15 (7%) DGCT, and 2/11 (18%) AOT cases. In comparison, conventional AM was positive for BRAF p.V600E mutation in 94% (17/18) of cases, while KRAS mutations were detected in 63% (7/11) of AOT cases. The study suggests that the so-called AA is a rare benign tumor that exhibits clinical, immunohistochemical, and molecular features similar to DGCTs. Based on these findings, AA should not be categorized as a standalone entity solely based on the presence of whorls/morules and cribriform/duct-like structures. Further studies are needed to investigate the pathologic mechanisms of these tumors and to identify potential therapeutic targets.

Modified Erchen decoction ameliorates cognitive dysfunction in vascular dementia rats via inhibiting JAK2/STAT3 and JNK/BAX signaling pathways.

BACKGROUND: Vascular dementia (VaD) is one of the most common clinical syndromes of progressive neurocognitive dysfunction with uncertain mechanisms. Modified Erchen decoction (MECD), developed from "Erchen decoction (ECD)" recorded in "Taiping Huimin Heji Jufang", showed a good effect in the treatment of VaD. However, its therapeutic mechanism is still unclear. PURPOSE: This study aimed to elucidate the multi-target mechanisms of MECD against VaD in vivo and in vitro. METHODS: VaD model was established by two-vessel obstruction (2-VO) in Sprague-Dawley rats. Six groups, including the control, 2-VO operation, MECD treatment (2.5, 5.0 and 10.0 g kg-1 d-1), donepezil hydrochloride (positive control, 0.45 g kg-1 d-1) were designed in the whole experiment. After oral administration for 4 weeks, the effects of MECD were verified by behavioral experiments, histological observation, and biochemical index analysis. The chemical profiling of MECD was performed by UHPLC-Orbitrap Fusion-HRMS, and a "compound-target-pathway" multivariate network was constructed to validate and elucidate its pharmacological mechanisms. RESULTS: Compared with 2-VO group, MECD treatment significantly alleviated anxiety and improved spatial memory in VaD rats according to the open field test (OFT) and Y-maze test. A significant increase in neuron number was observed from hematoxylin and eosin (H&E) stained images in cornu ammonis 1 (CA1) of the hippocampal region after MECD treatment. On the one hand, MECD reduced the plasma levels of triglyceride (TG), low-density lipoprotein (LDL), malondialdehyde (MDA), and amyloid-beta 42 (Aß42), and inhibited mRNA expression of interleukin-1 beta (Il-1ß) and Il-6 in the hippocampus. On the other hand, superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) were significantly increased after treatment with MECD. Moreover, MECD reduced the mRNA expression and protein expression of janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), c-Jun N-terminal kinase (JNK), and BCL2-associated X (BAX) in the brain of 2-VO rats. Furthermore, 71 compounds were identified from the extract of MECD. Among them, liquiritin and isochlorogenic acid C gave inhibiting effects on the mRNA expression of Jnk. In addition, liquiritin and hesperetin were conformed with the inhibition of Jak2 transcription level in vitro experiments. CONCLUSION: MECD has demonstrated a significant amelioration effect on cognitive dysfunction in VaD rats via JAK2/STAT3 and JNK/BAX signaling pathways, which represents an innovative insight into the "activate blood and eliminate phlegm" theory.

The prognostic impact of BMI on colorectal cancer is stratified by tumor location.

Purpose: Recent studies have revealed the contrasting prognostic roles of body mass index (BMI) and tumor location in colorectal cancer (CRC). Given that right- and left-sided CRC may exhibit inverse effects on outcome and body weight, the present study aimed to examine whether the prognostic value of BMI and tumor location could be reciprocally stratified. Methods: This prospective, observational study recruited 4,086 patients diagnosed with stage III CRC from five independent clinical centers in China. The association of patients' outcomes with BMI and tumor location was evaluated hierarchically by Kaplan-Meier and Cox proportional-hazards models. Results: Although BMI was not associated with overall outcome, the association was significantly modified by tumor location. Among left-sided tumors, obesity and overweight were significantly associated with adverse overall survival (OS) and disease-specific survival (DSS). In contrast, among right-sided tumors, overweight was significantly associated with more favorable OS and DSS compared with the normal-weight group. The association of survival with tumor location did not reach statistical significance. However, hierarchical analysis by BMI revealed that left-sided tumors were associated with more favorable outcomes in the normal-weight group, while there was no statistically significant difference in the overweight or obese group. Conclusions: BMI and tumor location may have opposing effects on CRC prognosis, when stratified by each other, after adjusting for other known prognostic factors. These findings are the first to show the interactive prognostic impact of BMI and tumor location, which could be relevant to the stratification of patient management.

Magnolol attenuates the locomotor impairment, cognitive deficit, and neuroinflammation in Alzheimer's disease mice with brain insulin resistance via up-regulating miR-200c.

In this study, we aimed to investigate the effect of Magnolol on Alzheimer's disease (AD). After the model of streptozotocin-induced AD mice with brain insulin resistance was established, the mice were treated with Magnolol or miR-200c antagomiR. The abilities of ambulations, rearings, discrimination, spatial learning, and memory were evaluated by open-field test (OFT), novel object recognition (NOR), and morris water maze (MWM) tests. The levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), and miR-200c in the mice hippocampus were evaluated by enzyme-linked immunosorbent assay, Western blot, or Quantitative real-time Polymerase Chain Reaction. In AD mice model, streptozotocin induced the locomotor impairment and cognitive deficit, up-regulated levels of MDA, TNF-α, IL-6, and CRP, while down-regulated levels of GSH, SOD, and miR-200c. Magnolol increased the rearings numbers and discrimination index of AD mice in OFT and NOR tests. Magnolol increased the number of entries in the target quadrant and time spent in the target quadrant and decreased the escape latency of AD mice in the MWM test. Magnolol also down-regulated the levels of MDA, TNF-α, IL-6, and CRP, and up-regulated the levels of GSH, SOD, and miR-200c in the hippocampus tissues of AD mice. However, miR-200c antagomiR did the opposite and further offset the effects of the Magnolol on AD mice. Magnolol attenuated the locomotor impairment, cognitive deficit, and neuroinflammatory in AD mice with brain insulin resistance via up-regulating miR-200c.

Delta-like ligand 4 level in colorectal cancer is associated with tumor aggressiveness and clinical outcome.

BACKGROUND: The Notch signaling regulates numerous cell growth, differentiation, and death. However, the expression pattern of its ligand Delta-like 4 (DLL4) in tumors is still uncertain. OBJECTIVE: In the present study, we examined DLL4 expression in colorectal cancer as well as assessed its role as a prognostic indicator in the present study. METHODS: DLL4 expression was examined by immunohistochemistry in 289 surgically resected specimens of colorectal cancer and adjacent normal tissues. The relationship between DLL4 expression and clinicopathological characteristics was analyzed. The association of DLL4 expression with the patients' overall survival rate was assessed by Kaplan-Meier and Cox proportional-hazards regression. RESULTS: Increased DLL4 level was detected in colorectal cancer compared with that of normal tissues. Elevated DLL4 level in colorectal cancer was associated with increased body mass index of patients. Moreover, increased DLL4 level was also found to be correlated with tumor invasion, metastases and unfavorable clinical outcom of patients. CONCLUSIONS: DLL4 level is increased in colorectal cancer, especially in patients with increased body mass index, indicating potential involvement of obesity-related tumorigenesis and development. It might also serve as a novel molecular marker to predicate outcome of patients.

[Effects of electroacupuncture on insulin resistance in patients with knee arthroplasty].

OBJECTIVE: To explore the effect of electroacupuncture on the improvement of insulin resistance after knee joint replacement based on the combined spinal and epidural anesthesia and postoperative epidural analgesia. METHODS: Eighty patients with insulin resistance but normal blood glucose were randomly divided into a control group and an observation group, 40 cases in each group.Both groups of patients underwent combined spinal and epidural anesthesia and postoperative epidural analgesia for knee arthroplasty. On the basis of the treatment,electroacupuncture (EA) was applied during the operation and within 1 month after the operation in the observation group, and EA was used at Hegu (LI 4), Qihai (CV 6), Zhongwan (CV 12), Pishu (BL 20), Shenshu (BL 23), etc. once every other day. The control group was not treated with electroacupuncture. Fasting blood glucose and fasting insulin were recorded 30 min before surgery (T0), immediately (T1), 1 d (T2), 3 d (T3), 7 d (T4) and 1 month (T5) after surgery, and the insulin resistance (IR) index was calculated. RESULTS: Compared with those at T0 time point, the IR index of the control group at T1, T3, T4 and T5 time points and the observation group at T1, T4, T5 time points were lower (all P<0.05). Compared with the control group at the same time point, the IR index of the T1 and T5 time points in the observation group was significantly lower (both P<0.05), and it was lower than the insulin resistance standard. CONCLUSION: Combined spinal and epidural anesthesia and postoperative epidural analgesia can improve short-term insulin resistance. Combined with EA, the improvement of insulin resistance is more obviously and longer.

Synthesis and Activity Evaluation of Nasopharyngeal Carcinoma Inhibitors Based on 6-(Pyrimidin-4-yl)-1H-indazole.

Human nasopharyngeal carcinoma is a common head and neck malignancy with high incidence in Southeast Asia and Southern China. It is necessary to develop safe, effective and inexpensive anticancer agents to improve the therapeutics of patients with nasopharyngeal carcinoma. A series of small molecular compounds based on 6-(pyrimidin-4-yl)-1H-indazole were synthesized and evaluated for antiproliferative activities against human nasopharyngeal carcinoma cell lines SUNE1. Compounds 6b, 6c, 6e and 6l showed potent antiproliferative activities similar to positive control drug cisplatin in vitro with lower nephrotoxicity than it. N-[4-(1H-Indazol-6-yl)pyrimidin-2-yl]benzene-1,3-diamine (6l) was selected for further study. It was found that 6l induced mitochondria-mediated apoptosis and G2 /M phase arrest in SUNE1 cells. Furthermore, compound 6l at 10 mg/kg can suppress the growth of an implanted SUNE1 xenograft with a TGI% (tumor growth inhibition) value of 50 % and did not cause serious side effects in BALB/c nude mice. This study suggests that 6-(pyrimidin-4-yl)-1H-indazole derivatives are a series of small molecule compounds with anti-nasopharyngeal carcinoma activities.

[Design and synthesis of imidazo-fused heterocycles derivatives and their anti-tumor activity against breast cancer in mice].

OBJECTIVE: To synthesize compounds based on imidazo-fused heterocycles and evaluate their anti-tumor activity against breast cancer. METHODS: The compounds 1a-1e, 2a and 2b were synthesized by aerobic copper-catalyzed halocyclization of methyl N-heteroaromatics with aliphatic amines; 3a and 3b were generated by sonogashira reaction and Suzuki reaction, respectively; the compounds 4a-4c were obtained by Buchwald-Hartwig reaction of the corresponding amines and 1e. The effects of these compounds against breast cancer cells and their nephrotoxicity were determined using MTT assay. Annexin VFITC/PI apoptosis detection kit was used to assess the apoptosis-inducing effects of these compounds in breast cancer cells. With normal saline as the control, the safety and anti-tumor activity of the compound 2a (daily dose of 10 mg/kg for 14 days) was tested in a mouse model bearing human breast cancer xenografts. RESULTS: The compounds 2a, 4a, 4b and 4c all showed obvious anti-tumor activities. Among these compounds, 2a showed the most potent anti-tumor effect against breast cancer cells with an IC50 of 9.77 ± 2.32 µmol/L, similar to that of cisplatin (IC50=8.96 ± 2.35 µmol/L); 2a also showed a slightly lower nephrotoxicity than cisplatin, and their CC50 was 10.79±0.87 µmol/L and 8.45±0.68 µmol/L, respectively. 2a obviously promoted apoptosis of breast cancer cells in vitro and caused a moderate suppression of the breast cancer growth in the tumor-bearing mouse models without producing serious adverse effects. CONCLUSIONS: Four compounds synthesized based on imidazo-fused heterocycles have anti-tumor activities against breast cancer. The compound 2a is capable of dose-dependently promoting apoptosis of breast cancer cells in vitro and has a good safety and a moderate efficacy for suppressing tumor growth in mouse models bearing human breast cancer xenografts.

Elucidation of the Intestinal Absorption Mechanism of Loganin in the Human Intestinal Caco-2 Cell Model.

Loganin, iridoid glycosides, is the main bioactive ingredients in the plant Strychnos nux-vomica L. and demonstrates various pharmacological effects, though poor oral bioavailability in rats. In this study, the intestinal absorption mechanism of loganin was investigated using the human intestinal Caco-2 cell monolayer model in both the apical-to-basolateral (A-B) and the basolateral-to-apical (B-A) direction; additionally, transport characteristics were systematically investigated at different concentrations, pHs, temperatures, and potential transporters. The absorption permeability (PappAB) of loganin, which ranged from 12.17 to 14.78 × 10-6cm/s, was high at four tested concentrations (5, 20, 40, and 80µM), while the major permeation mechanism of loganin was found to be passive diffusion with active efflux mediated by multidrug resistance-associated protein (MRP) and breast cancer resistance protein (BCRP). In addition, it was found that loganin was not the substrate of efflux transporter P-glycoprotein (P-gp) since the selective inhibitor (verapamil) of the efflux transporter exhibited little effects on the transport of loganin in the human intestinal Caco-2 cells. Meanwhile, transport from the apical to the basolateral side increased 2.09-fold after addition of a MRP inhibitor and 2.32-fold after addition of a BCRP inhibitor. In summary, our results clearly demonstrate, for the first time, a good permeability of loganin in the human intestinal Caco-2 cell model and elucidate, in detail, the intestinal absorption mechanism and the effects of transporters on iridoid glycosides compounds.

Lin28b and Sox2 regulate anesthesia-induced neural degeneration in neural stem cell derived neurons.

Ketamine, a commonly used anesthetic compound, may cause neurotoxicity in immature or developing brains. In this study, we indented to understand the molecular expression and functional role of Lin-28 Homolog B (lin28b) in regulating ketamine-induced neurotoxicity in neural stem cells (NSCs)-differentiated neurons. NSCs from embryonic rat brains were cultured in vitro, and induced toward neuronal differentiation. NSCs-differentiated neurons were treated with various concentrations of ketamine for 24h to evaluate the concentration-dependent effect of ketamine on endogenous lin28b mRNA level. QRT-PCR showed that lin28b was downregulated by ketamine in NSCs-differentiated neurons, in concentration-dependent manner. Neurons were then transfected with adenovirus to ectopically upregulate lin28b. We found that ketamine-induced apoptosis and neurite retraction in NSCs-differentiated neurons were significantly reduced by adenovirus-mediated lin28b upregulation. Expression of sex determining region Y box 2 (Sox2) mRNA was examined in ketamine-injured and lin28b-upregulated NSCs-differentiated neurons. It was found Sox2 was downregulated by ketamine, and overexpressed by lin28b upregulation. Finally, Sox2 was downregulated by siRNA in NSCs-differentiated neurons. And we discovered that Lin28b-upregulation-associated neural protection was severely hampered by Sox2 downregulation in ketamine-injured neurons. Thus, Lin28b and Sox2 are important molecular components in ketamine-induced neurotoxicity.

Involvement of spinal SIRT1 in development of chronic constriction injury induced neuropathic pain in rats.

It is known that the epigenetic process of histone acetylation is involved in the neuropathic pain. The aim of this study was to determine whether sirtuin type 1 (SIRT1), an NAD+ dependent deacetylase, affected allodynia and hyperalgesia in neuropathic pain. The neuropathic pain model was established by ligature of the right sciatic nerve to induce chronic constriction injury (CCI) in rats. Histone acetyltransferase (HAT) activity was increased and, and histone deacetylase (HDAC) activity was declined in tissue of the spinal dorsa horn in CCI rates by means of enzyme-linked immunosorbent assay (ELISA). The persistent hyperalgesia and allodynia caused by CCI were associated with downregulation of SIRT1 and upregulation of acetylated-H3 (Ac-H3) in tissue of the spinal cord by Western blot assay, which was reversed after intrathecal injection of SIRT1 agonist SRT1720. SRT1720 treatment achieved analgesic through inhibiting the acetylation of nuclear factor kappa B (NF-κB) and blocking the releases of the inflammatory factors including tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 by means of Western blot and real-time quantitative PCR (RT-PCR), respectively. Taken together, these data suggest that SIRT1 in the spinal cord plays an important role in the neuropathic pain in the rat model.

[Effects of auricular point sticking on plasma motilin in patients after gynecological laparoscopic operation under general anesthesia].

OBJECTIVE: To observe the clinical efficacy of auricular point sticking on prevention and treatment of gastrointestinal complications after gynecological laparoscopic operation of general anesthesia, and to explore whether it is achieved by regulating the secretion of plasma motilin (MTL). METHODS: Sixty patients who received selective gynecological laparoscopy under general anesthesia were randomly assigned into an observation group and a control group, 30 patients in each one. The patients in the observation group were treated with auricular point sticking at each morning and night, 30 min before anesthesia, revival after surgery and 24 h after surgery. The adhesive fabric with vaccaria seeds was pressed at shenmen (TF4), wei (CO4), benmen (CO3), jiaogan (AH6a) and pizhixia (AT4) for 3 to 5 min until the sensation of sourness, distension and numb appeared. The treatment was given for one week. The patients in the control group were treated only with similar adhesive fabric at auricular points at identical time points; each auricular point was pressed for 3 to 5 min. The anus exhaust time, defecating time and borborygmus were recorded; the level of plasma MTL was tested 30 min before anesthesia, 24 h after o-peration and 48 h after operation; the occurrence of nausea and vomiting from the end of operation to the end of treatment were also recorded. RESULTS: Compared with the control group, the occurrence of nausea after operation was reduced in the observation group (P<0.05), and the anus exhaust time and defecating time were shortened (both P<0.05), and the recovery of borborygmus was improved (P<0.05). The levels of MTL 24 h and 48 h after surgery were higher than those before operation in the two groups (all P<0.05); The levels of MTL 24 h and 48 h after surgery in the observation group were significantly lower than those in the control group (both P<0.05). CONCLUSIONS: The assist of auricular point sticking could reduce the occurrence of nausea-vomiting and accelerate the recovery of gastrointestinal function in gynecological laparoscopic operation under general anesthesia, which is likely to be related with the inhibition on excess secretion of MTL.

Inhibition of hypoxia and serum deprivation-induced apoptosis by salvianolic acid in rat mesenchymal stem cells.

OBJECTIVE: To investigate the influence and mechanism of salvianolic acid B (SalB) on apoptosis inhibition in rat bone marrow-derived mesenchymal stem cells (BMSCs) induced by hypoxia and serum deprivation (hypoxia/SD). METHODS: SalB concentration of 0.1, 1, 10 or 100 mg/L (drug groups) were investigated for their ability to inhibit apoptosis in rat BMSCs. BMSCs in both the apoptosis model and drug groups were cultured under hypoxic conditions for 6 h, after which cell apoptosis and change in mitochondrial membrane potential (MMP) were detected using flow cytometry. Activation of caspase-3 was detected using western blot analysis. RESULTS: Hypoxia/SD induced apoptosis in rat BMSCs. The early apoptosis rate was lower in the drug groups compared to the apoptosis model group (P < 0.05). SalB was found to inhibit the reduction in MMP and decrease the activation of caspase-3. CONCLUSION: 0.1, 1 and 10 mg/L of SalB inhibits activation of caspase-3 and early apoptosis of rat BMSCs induced by hypoxia/SD and could therefore enhance the survival rate of grafted stem cells.

Current progress of research on pharmacologic actions of salvianolic acid B.

As one of the main water-soluble composites of Radix Salviae, salvianolic acid B is a phenolic acid ingredient of the Chinese drug, which is rich content in the herb and has strong pharmaceutical activity. It is used to treat cardiocerebral vascular diseases, antagonize hepatic/renal fibrosis, prevent cancer, and promote stem cell proliferation and differentiation. In the researches of its acting mechanisms, rather deepened studies have been carried out for its application on cardiocerebral vascular diseases, but that for others are rather fewer.