ABSTRACT
Objective: To analyze the incidence of preterm birth based on pre-pregnancy body mass index (BMI) stratification and explore the associated factors of preterm birth among pregnant women at different BMI stratifications. Methods: From February 2018 to December 2020, pregnant women who participated in China Birth Cohort Study (CBCS) and gave birth at Beijing Obstetrics and Gynecology Hospital were enrolled as the study subjects. Electronic Data Capture System and standard structured questionnaires were used to collect data related to pre-pregnancy, pregnancy, and delivery for pregnant women. Pregnant women were divided into the low-weight group, normal-weight group and overweight group based on their pre-pregnancy BMI. A Cox proportional hazards model was used to analyze the associated factors of preterm birth among pregnant women with different BMI before pregnancy. Results: A total of 27 195 singleton pregnant women were included, with a preterm birth rate of 5.08% (1 381/27 195). The preterm birth rates in the low-weight group, normal-weight group and overweight group were 4.29% (138/3 219), 4.63% (852/18 390) and 7.00% (391/5 586) respectively (P<0.001). After adjusting for relevant factors, the Cox proportional hazards model showed that the risk of preterm birth in the overweight group was 1.457 times higher than that in the normal-weight group (95%CI: 1.292-1.643). Preeclampsia-eclampsia (HR=2.701, 95%CI: 1.318-5.537) was the associated factor for preterm birth in the low-weight group. Advanced maternal age (HR=1.232, 95%CI: 1.054-1.441), history of preterm birth (HR=4.647, 95%CI: 3.314-6.515), vaginal bleeding in early pregnancy (HR=1.613, 95%CI: 1.380-1.884), and preeclampsia-eclampsia (HR=3.553, 95%CI: 2.866-4.404) were associated factors for preterm birth in the normal-weight group. Advanced maternal age (HR=1.473, 95%CI: 1.193-1.818), history of preterm birth (HR=3.209, 95%CI: 1.960-5.253), vaginal bleeding in early pregnancy (HR=1.636, 95%CI: 1.301-2.058), preeclampsia-eclampsia (HR=2.873, 95%CI:2.265-3.643), and pre-gestational diabetes mellitus (HR=1.867, 95%CI: 1.283-2.717) were associated factors for preterm birth in the overweight group. Conclusion: Pre-pregnancy overweight is an associated factor for preterm birth, and there are significant differences in the associated factors of preterm birth among pregnant women with different BMI before pregnancy.
Subject(s)
Pregnancy , Infant, Newborn , Female , Humans , Body Mass Index , Overweight/epidemiology , Premature Birth/epidemiology , Pre-Eclampsia/epidemiology , Cohort Studies , Eclampsia , Incidence , Risk Factors , Thinness/epidemiologyABSTRACT
Objective: To explore the association between coagulation function indicators and placental abruption (PA) in different trimesters of pregnancy among preeclampsia-eclampsia pregnant women. Methods: From February 2018 to December 2020, pregnant women who participated in the China birth cohort study and were diagnosed with preeclampsia, eclampsia and chronic hypertension with superimposed preeclampsia in Beijing Obstetrics and Gynecology Hospital were enrolled in this study. The baseline and follow-up information were collected by questionnaire survey, and the coagulation function indicators in the first and third trimesters were obtained through medical records. The Cox proportional hazards model was used to analyze the association between the coagulation function indicators and PA. A restrictive cubic spline curve was used to draw the dose-response curve between the relevant coagulation function indicators and PA. Results: A total of 1 340 participants were included in this study. The age was (32.50±4.24) and the incidence of PA was 4.4% (59/1 340). After adjusting for relevant factors, Cox proportional hazards model showed that compared with the high-level classification of fibrinogen (FIB), participants within the middle-(HR=3.28, 95%CI: 1.27-8.48) and low-level (HR=3.84, 95%CI: 1.40-10.53) classification during the first trimester and within the low-level classification (HR=4.18, 95%CI: 1.68-10.39) during the third trimester were more likely to experience PA. Compared with the middle-level classification of pro-thrombin time (PT), the risk of PA in the participants within the low-level classification (HR=2.67, 95%CI: 1.48-4.82) was significantly higher in the third trimester. The restrictive cubic spline analysis showed a linear negative association between FIB and PA in the first and third trimesters, while PT and PA showed an approximately L-shaped association . Conclusion: Among pregnant women diagnosed with preeclampsia-eclampsia, the middle-and low-level classification of FIB in the first and third trimesters and the low-level classification of PT in the third trimester could increase the risk of PA.
Subject(s)
Pregnancy , Female , Humans , Pre-Eclampsia/diagnosis , Abruptio Placentae/epidemiology , Pregnant Women , Eclampsia , Cohort Studies , PlacentaABSTRACT
The transcription factor X-box binding protein-1 (XBP1) plays a key role in unfolded protein reaction. This study was aimed to investigate the expression pattern and regulation of XBP1 in the mouse uterus during early pregnancy. The methods of immunohistochemistry (IHC) and real time quantitative RT-PCR were used to test XBP1 expression in early pregnancy, artificial decidualization, oestrous cycle and hormone-regulated mouse models. The results showed that XBP1 was spatiotemporally expressed in mouse uterus during early pregnancy. The XBP1 protein was mainly detected in the luminal and glandular epithelia on days 1-4 of pregnancy, and was strongly detected in the decidual area on days 5-8 of pregnancy. Similarly, XBP1 expression was also mainly expressed in decidual cells following artificial decidualization. During the oestrous cycle, Xbp1, Xbp1u, and Xbp1s mRNA was predominantly present in proestrus. In the ovariectomized uterus, the expression of XBP1 in luminal and glandular epithelia was up-regulated after estrogen treatment. These results suggest that XBP1 is associated with embryo implantation and decidualization during early pregnancy in mice, and the expression of XBP1 in luminal and glandular epithelia may be regulated by estrogen.
Subject(s)
Animals , Female , Mice , Pregnancy , Decidua , Embryo Implantation , Estrogens , RNA, Messenger/genetics , UterusABSTRACT
BACKGROUND:Collagen-bioglass-polycaprolacton (COL-BG-PCL) composites have good biocompatibility, mechanical properties and biodegradability that are beneficial to cell adhesion, proliferation and angiogenesis. OBJECTIVE:To study the effect of COL-BG-PCL bioactive scaffold on the proliferation, migration and differentiation of human dental pulp cells (hDPCs). METHODS:hDPCs were isolated and cultured on the COL-BG-PCL bioactive scaffold. MTT, cell scratch test and enzyme-linked immunosorbent assay (ELISA) assay were used to detect the proliferation, migration and differentiation abilities of hDPCs before and at 1, 3, 7, 14, 24 days after inoculation onto the COL-BG-PCL bioactive scaffold. RESULTS AND CONCLUSION:Compared with the cells without inoculation onto the COL-BG-PCL bioactive scaffold, (1) the proliferation ability of the cells cultured on the COL-BG-PCL scaffold was significantly enhanced (P<0.01), and with the prolongation of the inoculation time, the cell proliferation ability was gradually increased; (2) the cell migration ability of the cells cultured on the COL-BG-PCL scaffold was significantly enhanced (P<0.01), and with the prolongation of the inoculation time, the migration ability of the cells cultured on the COL-BG-PCL scaffold was gradually increased; (3) the level of alkaline phosphatase in the supernatant of the cells cultured on the COL-BG-PCL scaffold was significantly increased (P<0.01), and with the prolongation of the inoculation time, the level of alkaline phosphatase in the supernatant was gradually increased. In summary, the COL-BG-PCL scaffold can promote the proliferation, migration and differentiation of hDPCs.
ABSTRACT
Rapid allele-specific PCR primer was designed base on Cytb 155 A/T single nucleotide polymorphism, DNA was extracted by alkaline lysis and the PCR reaction systems including denatured and annealing temperature and cycle numbers were optimized. The results were performed to authenticate Ranae Oviductus and its 4 adulterants. When 100×SYBR Green I was added in the PCR product at 90 ℃ denatured 3 s, 62 ℃ annealing 20 s and 32 cycle. Ranae Oviductus visualized strong green fluorescence under 365 nm UV lamp whereas adulterants appeared negative. The whole process can be completed in 40 minutes.The established method provides the technical support for authentication of the Ranae Oviductus.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the impact of the BKCa channel in prostate smooth muscle cells (PSMCs) on the membrane potential in SD rats with chronic abacterial prostatitis (CAP).</p><p><b>METHODS</b>CAP models were established in 20 SD rats by castration and injection of 17 beta-estrogen, and another 20 were taken as normal controls. PSMCs were cultured and purified in vitro, and treated with DiBAC4, followed by quantitative observations on the dynamic changes of the cell membrane potential by laser confocal microscopy.</p><p><b>RESULTS</b>The extracellular calcium ion concentration ([Ca2+]o) was increased and the BKCa channel was activated, which induced the hyperpolarization of the PSMC membrane in both the CAP models and normal control rats. This effect was weakened with Iberiotoxin (IbTX), a specific blocker of the BKCa channel, but the amplitude of the hyperpolarization was obviously lower in the CAP than in the control group. The DiBAC4 fluorescence intensity induced by hyperpolarization was 18.78 +/- 2.92 in the former and 38.85 +/- 7.10 in the latter (P < 0.05), while that induced by IbTX was 1.61 +/- 0.46 and 6.12 +/- 1.32 (P < 0.05), respectively.</p><p><b>CONCLUSION</b>Significant decrease of BKCa-mediated hyperpolarization in the CAP model can reduce its abilities of regulating the membrane potential and suppressing the excessive contraction of PSMCs, which may result in pelvic pain syndrome and lower urinary tract symptoms.</p>
Subject(s)
Animals , Male , Rats , Cells, Cultured , Large-Conductance Calcium-Activated Potassium Channel alpha Subunits , Membrane Potentials , Myocytes, Smooth Muscle , Cell Biology , Metabolism , Potassium Channels , Metabolism , Prostate , Cell Biology , Prostatitis , Metabolism , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of Panax notoginseng (PN) on pathological features in chronic subdural hematoma (CSDH) rabbits and its mechanisms.</p><p><b>METHODS</b>A stable pathological animal model similar to CSDH in humans could be established using subdural injections of small number of blood through a subdural pre-catheter in rabbits. After successful modeling, 18 rabbits were randomly divided into the model group, the low dose PN group (0.125 g/kg), and the high dose PN group (0.250 g/kg), 6 in each group. Normal saline was given to rabbits in the model group, while PN power was given to those in the PN groups by gastrogavage for 6 successive days. Pathologic features of the hematoma outer membrane were observed by HE staining. The activity of SOD and the content of MDA in the hematoma outer membrane were examined by the colorimetric method. Expressions of CD31, CD34, and VEGF in the hematoma outer membrane were observed by immunohistochemical assay. Expressions of VEGF in the peripheral blood and the subdural hematoma were detected by enzyme-linked immunosorbent assay (ELISA). Expressions of VEGFR-1 and VEGFR-2 in the hematoma outer membrane were detected by Western blot.</p><p><b>RESULTS</b>Compared with the model group, the inflammatory reaction was comparatively lessen and the proliferation of the fibrous tissue was relatively mature in the low and high dose PN groups. The activity of SOD increased (P < 0.05); expressions of CD31 and CD34 were reduced (P < 0.01); VEGF expression in the residual hematoma fluid decreased (P < 0.05) in the high dose PN group. Expressions of VEGF and VEGFR-2 were all reduced in the high and low dose PN groups (P < 0. 05, P < 0.01). Compared with the low dose PN group, expressions of CD31 and CD34 were reduced (P < 0.01), and the VEGFR-2 expression was also reduced (P < 0.05) in the high dose PN group.</p><p><b>CONCLUSIONS</b>PN could promote the fibrous repairing of subdural hematoma in CSDH rabbits. It also lessened inflammation and oxidative injury of the hematoma outer membrane and reduced expressions of VEGF. The pathological angiogenesis could be reduced through influencing VEGFR-2 receptor pathways, which might be an important mechanism.</p>
Subject(s)
Animals , Rabbits , Disease Models, Animal , Drugs, Chinese Herbal , Pharmacology , Hematoma, Subdural, Chronic , Metabolism , Pathology , Panax notoginseng , Chemistry , Vascular Endothelial Growth Factor A , Metabolism , Vascular Endothelial Growth Factor Receptor-1 , Metabolism , Vascular Endothelial Growth Factor Receptor-2 , MetabolismABSTRACT
<p><b>AIM</b>To explore the effect of baicalein (Bai-Chinese Traditional Medicine) on bleomycin (BLM)-induced fibrosis in lungs of rats and its possible mechanism.</p><p><b>METHODS</b>Sixty-eight male Sprague-Dawley rats were randomly divided into 4 groups: BLM plus Bai group, BLM plus normal saline (NS) group, NS plus Bai group, and NS plus NS group. The rats were received single intratracheal instillation of BLM (5 mg kg(-1) bw) or equal volume of NS as control, and received intraperitoneal injection o f Bai (12.5 mg x kg(-1) bw) or the same volume of NS asvehicle for 28 d. The hydroxyproline content, the collagen area, the mRNA expression of Col I (alpha), and the myofibroblasts in lung were examined.</p><p><b>RESULTS</b>The content of hydroxyproline, the percentage of collagen area, the mRNA expression of Col I (alpha), and the amount of myofibroblast were increased in lungs of rats on day 28 after intratracheal instillation of BLM, compared with that in lungs of the control rats, respectively( All P < 0.01). The above abnormal changes were ameliorated by Bai (12.5 mg x kg(-1) x d(-1) ip, x 28 d (All P < 0.05).</p><p><b>CONCLUSION</b>Bai has anti-action on BLM-induced fibrosis in lung, and that the above action of Bai is related to the blockage of synthesis of type I collagen and the decrease of myofibroblast in lung.</p>
Subject(s)
Animals , Male , Rats , Bleomycin , Collagen Type I , Genetics , Metabolism , Flavanones , Pharmacology , Therapeutic Uses , Myofibroblasts , Cell Biology , Pulmonary Fibrosis , Drug Therapy , RNA, Messenger , Genetics , Metabolism , Random Allocation , Rats, Sprague-DawleyABSTRACT
<p><b>BACKGROUND</b>A number of studies have shown that oxidative stress and mitochondrial involvement are major triggering factors in the development of neurodegenerative diseases. Cobalt chloride (CoCl(2))-induced cell death in PC12 cells may serve a simple and convenient in vitro model of hypoxia-induced neuronal cytotoxicity. To explore the effect of geniposide on CoCl(2) which induced cytotoxicity and mitochondrial function in rat pheochromocytoma PC12 cells, we analyzed the influence of geniposide on the expression of apoptosis-related proteins.</p><p><b>METHODS</b>PC12 cells and RNAi PC12 cells were treated with 0, 12.5, 25, 50, 100 micromol/L geniposide for 12 hours and then exposure to 400 micromol/L CoCl(2) for 12 hours. Cell viability, cell morphology, and expression of Bcl-2, Bax, P53 and caspase-9 were determined using Western blotting.</p><p><b>RESULTS</b>Pretreatment with geniposide markedly improved the cells viability and morphology, decreased the expression of Bax, P53 and caspase-9, and increased the expression of Bcl-2 in PC12 cells challenged by CoCl(2)2. However, in the RNAi PC12 cells, geniposide had no significant effect on the expression of these proteins.</p><p><b>CONCLUSION</b>Geniposide protects PC12 cells from CoCl(2) involved in mitochondrial mediated apoptosis, and GLP-1R might play a critical role in the neuroprotection of geniposide in PC12 cells.</p>
Subject(s)
Animals , Rats , Apoptosis , Cobalt , Toxicity , Glucagon-Like Peptide-1 Receptor , Iridoids , Pharmacology , Mitochondria , Physiology , Neuroprotective Agents , Pharmacology , PC12 Cells , Proto-Oncogene Proteins c-bcl-2 , Physiology , Receptors, Glucagon , Physiology , Signal Transduction , bcl-2-Associated X Protein , PhysiologyABSTRACT
<p><b>OBJECTIVE</b>To study the effect of total glucosides of paeony (TGP) on lipopolysaccharides (LPS)-induced nuclear factor-kappaB (NF-kappaB) activation in macrophages.</p><p><b>METHOD</b>Rat peritoneal macrophages were pre-treated with TGP for 2 h and stimulated with LPS for 20 min or 0.5 h. Inhibitory kappaBalpha (IkappaBalpha) protein in the cytoplasm and NF-kappaB p65 protein in the nuclear were analyzed by western blot. Further, DNA binding activity of NF-kappaB complex was detected.</p><p><b>RESULT</b>TGP enhanced the amounts of IkappaBalpha protein in the cytoplasm and decreased the amounts of NF-kappaB p65 protein in the nuclear of LPS-induced macrophages. TGP also inhibited the LPS-mediated DNA binding activity of NF-kappaB complex in macrophages.</p><p><b>CONCLUSION</b>TGP can inhibit LPS-induced NF-kappaB activation in macrophages through arresting IKBalpha protein degradation, NF-kappaB p65 protein nuclear translocation and DNA binding activity of NF-kappaB complex.</p>
Subject(s)
Animals , Rats , Cell Nucleus , Metabolism , Cytoplasm , Metabolism , DNA , Metabolism , Dose-Response Relationship, Drug , Glucosides , Pharmacology , Macrophages, Peritoneal , Cell Biology , Metabolism , NF-kappa B , Metabolism , Paeonia , Chemistry , Protein Transport , Transcription Factor RelA , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the change of JNK and c-Jun in lung injury associated with paraquat poisoning of rats.</p><p><b>METHODS</b>46 Rats were randomly divided into four groups: PQ group (n = 12), control group (n = 10), PQ + ZnPP group (n = 12) and PQ + Hm group (n = 12). The rats were injected with 2% PQ (25 mg/kg, ip) in PQ group. ZnPP and Hemin (10 mg/kg, 10 mg/ml) were injected through inguinal vein before intraperitoneal administration of 2% paraquat in PQ + ZnPP group and PQ + Hm group respectively. The rats were injected NS (1 ml/kg, ip) in control group. HE dyeing of lung tissue and MDA content of plasma were used for estimating the injury of lung tissue. The content of CO in the lung tissue was determined. The expression of HO-1 mRNA of the lung tissue was detected by the reverse transcription-polymerase chain reaction. The phosphorylation of JNK and c-Jun was evaluated by Western blot analysis.</p><p><b>RESULTS</b>The degree of lung injury in PQ group and PQ + ZnPP group was higher than that in control group and PQ + Hm group. But in PQ + Hm group the degree of lung injury was lower. The content of MDA in PQ group and PQ + ZnPP group was higher than that in control group and PQ + Hm group (P < 0.01). The content of MDA in PQ + Hm group was higher than that in control group (P < 0.05). The content of CO in lung tissue in PQ group, PQ + ZnPP group and PQ + Hm group was and (1.08 +/- 0.15 mg/L) respectively, and higher than that in control group (P < 0.01). The content of CO in lung tissue in PQ + Hm group was significantly higher than that in PQ + ZnPP group (P < 0.01). The expression of HO-1 and the phosphorylation of JNK (55.24 +/- 9.34, 38.15 +/- 10.71, 128.55 +/- 19.43) and c-Jun (23.16 +/- 4.85, 15.49 +/- 3.13, 44.89 +/- 10.37) were increased remarkably in PQ group, PQ + ZnPP group and PQ + Hm group. Those in PQ + Hm group were higher significantly than PQ group and PQ + ZnPP group (P < 0.01). Those in PQ + ZnPP group were lower than PQ group (P < 0.05).</p><p><b>CONCLUSION</b>The increase of CO of lung tissue in rats at the lung injury associated with paraquat poisoning reduces the acute lung injury of rats. The level of JNK and c-Jun phosphorylation increases obviously, especially after Hemin is utilized.</p>
Subject(s)
Animals , Male , Rats , Acute Lung Injury , Metabolism , Disease Models, Animal , JNK Mitogen-Activated Protein Kinases , Metabolism , Lung , Metabolism , Paraquat , Poisoning , Proto-Oncogene Proteins c-jun , Metabolism , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To evaluate the efficacy and safety of cluster immunotherapy with Dermatophagoides pteronyssinus for allergic rhinitis.</p><p><b>METHODS</b>One hundred and fifty-four patients with allergic rhinitis to Dermatophagoides pteronyssinus were allocated to receive specific immunotherapy in a 6-week cluster schedule during the incremental-dose phase. Thereafter, these patients received maintenance-dose injection at 6-week intervals until the end of 1 year of treatment. Symptom scores and medication scores were used to evaluate the clinical efficacy and adverse reactions were recorded. A rhinoconjunctivitis quality of life questionnaire (RQLQ) was completed in the baseline and after one year treatment.</p><p><b>RESULTS</b>Cluster immunotherapy significantly reduced the symptom scores and total medication score of patients enrolled (P < 0.01). The immunotherapy group also had a significant improvement in the Rhinoconjunctivitis Quality of Life Questionnaire. During the one-year of treatment, there were 26 systemic adverse reactions (0.75% of all injection) in 9 patients (5.9%) and no fatal systemic reactions occurred.</p><p><b>CONCLUSIONS</b>The cluster immunotherapy is efficacious and safe to treat allergic rhinitis.</p>
Subject(s)
Adolescent , Adult , Animals , Child , Female , Humans , Male , Middle Aged , Young Adult , Allergens , Antigens, Dermatophagoides , Allergy and Immunology , Dermatophagoides farinae , Allergy and Immunology , Immunotherapy , Rhinitis , Parasitology , Therapeutics , Treatment OutcomeABSTRACT
<p><b>OBJECTIVE</b>To evaluate the protective effect of high dose ambroxol, a mucoactive drug, on acute lung injury caused by paraquat in rats.</p><p><b>METHODS</b>One hundred and thirty-six healthy male Sprague-Dawley rats were randomly divided into three groups: control group (n = 24) injected with normal saline intraperitoneally, PQ group (n = 56) [(2% paraquat (25 mg/kg) injected into peritoneal cavity on the first day)] and AT group (n = 56) ambroxol 35 mg/kg was injected into peritoneum daily after paraquat intoxication once daily for 7 consecutive days. The arterial gas was determined and the extent of lung injury was assessed by measuring the ratio of wet to dry weight (W/D) and protein content in BALF, the WBC count, the percentage of PMN, the content of malondialdehyde (MDA) and the levels of superoxide dismutase (SOD) in the blood and BALF respectively. Left lung tissue was observed through both light microscope and electron microscope (TEM).</p><p><b>RESULTS</b>The white cell count and the content of protein in the blood and the BALF of PQ group were significantly higher than those of the control group (P < 0.05 or P < 0.01). On the 7th day, the content of MDA 9 [(8.12 +/- 1.12) nmol/ml] in the serum of PQ group was significantly higher than the control group and the GSH-Px activity [(1256.8 +/- 133.2) U/ml] was significantly lower than the control group (P < 0.01). The white cell count and the content of protein in the blood and the BALF of AT group were significantly lower than the PQ group (P < 0.05 or P < 0.01). On the 7th day, the content of MDA in the serum of the AT group [(4.86 +/- 0.75) nmol/ml] was significantly lower than the PQ group and the GSH-Px activity [(1509.5 +/- 183.0) U/ml] and the SOD activity [(3903.2 +/- 374.7) U/ml] were significantly higher than the PQ group (P < 0.01). Under optical and electronic microscopes, the injury of lung tissue was reduced after large dose of ambroxol was administered.</p><p><b>CONCLUSION</b>Treatment with ambroxol (35 mg/kg) could influence the status of oxidative stress in lung and alleviate lung injury induced by paraquat. Ambroxol has obviously therapeutic effect on paraquat poisoning.</p>
Subject(s)
Animals , Male , Rats , Acute Lung Injury , Drug Therapy , Metabolism , Pathology , Ambroxol , Pharmacology , Therapeutic Uses , Disease Models, Animal , Lung , Metabolism , Pathology , Oxidative Stress , Paraquat , Poisoning , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To investigate the influence of ambroxol on paraquat poisoning induced acute lung tissue injury and the change of pulmonary surfactant associated protein A in the experimental rats.</p><p><b>METHODS</b>One hundred and twenty healthy adult male Sprague-Dawley rats were randomizedly assigned into normal saline (NS) group (n = 24), paraquat poisoning induced lung tissue injury model (PQ) group (n = 48) and ambroxol treatment (AT) group (n = 48). The indexes were observed among the three groups comprising the mortality rate, the change of arterial blood PaCO(2) and PaO(2), the ratio of wet to dry lung tissue (W/D), the change of the lung tissue under light and electric microscope respectively, and the expression of pulmonary surfactant associated protein A.</p><p><b>RESULTS</b>The mortality rate of rats in the PQ group was 50.0% on the seventh day while the mortality rate in the AT group was 25.0%. The level of arterial blood PaCO(2) in the PQ group (6.94 +/- 0.8) kPa was significantly higher than that in the AT group (6.12 +/- 0.5) kPa and the NS group (4.6 +/- 0.4) kPa. The level of arterial blood PaO(2) in the PQ group (6.98 +/- 1.1) kPa was significantly lower than that in the AT group (8.25 +/- 0.7) kPa and the NS group (12.7 +/- 0.8) kPa. There were significant differences among the groups (P < 0.05). The degree of lung tissue injury was severe in PQ group and relieved in AT group. The expression of pulmonary surfactant associated protein A was significantly decreased in PQ group 13.22% +/- 2.21% on the seventh day, compared with that in the AT group (21.82% +/- 3.67%) (P < 0.05). The expression of pulmonary surfactant associated protein A in AT group was significantly higher in the AT group (18.97% +/- 0.91%) than that in the PQ group on the seventh day (P < 0.05).</p><p><b>CONCLUSION</b>Ambroxol plays a role in facilitating synthesis and secretion of pulmonary surfactant protein A and relieves the lung tissue injury induced by paraquat poisoning.</p>
Subject(s)
Animals , Male , Rats , Ambroxol , Pharmacology , Immunohistochemistry , Lung , Metabolism , Pathology , Paraquat , Poisoning , Pulmonary Surfactant-Associated Protein A , Random Allocation , Rats, Sprague-Dawley , Respiratory Distress Syndrome , Metabolism , PathologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of baicalin (Bai) on lung injury, the level of TNF-alpha in cultured liquid of pulmonary interstitial macrophage and the expression of heme oxygenase-1 (HO-1) in lung injury associated with paraquat poisoning.</p><p><b>METHODS</b>Rats were randomizedly divided into four groups: control group, PQ group, Bai group (Bai, 300 mg.kg(-1).d(-1)) and simple Bai group (Bai, 300 mg. kg(-1).d(-1)) (n = 10 in each group). The 2% PQ was injected (25 mg/kg) in PQ group. Bai was injected in the rats (300 mg.kg(-1).d(-1) x 3 d) through caudal vein after paraquat poisoning in Bai group. In simple Bai group, Bai was injected in the healthy rats (300 mg.kg(-1).d(-1) x 3 d). The samples were obtained three days after intraperitoneal administration of 2% paraquat (25 mg/kg). The injury of lung was estimated with HE dyeing and electron microscope. Pulmonary interstitial macrophage (PIM) were obtained, and then cultured for 24 hours. The content of TNF-alpha was evaluated. The expression of HO-1 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). The expression of HO-1 protein was evaluated by Western blot analysis.</p><p><b>RESULTS</b>The lung tissue was normal in control group and simple Bai group. The degree of lung injury in PQ group was higher than that in control group by HE dyeing and electron microscope observation. The level of TNF-alpha expression in cultured PIM in Bai group [(484.2 +/- 39.5) microg/L] was lower than that in PQ group [(790.2 +/- 35.0) microg/L], but higher than that in the control group [(121.6 +/- 19.2) microg/L] (P < 0.05). The expression of HO-1 mRNA and protein [(59.8 +/- 5.40) and (122.0 +/- 31.98)] in Bai group were higher than those in PQ group [(45.9 +/- 5.82) and (77.92 +/- 10.23)] (P < 0.05).</p><p><b>CONCLUSION</b>The lung injury associated with paraquat poisoning was alleviated by baicalin, which was possibly related to the decrease of level of TNF-alpha in cultured PIM and the increase of the expression of HO-1 mRNA and protein.</p>