Perceived control, self-management efficacy, and quality of life in patients treated with radiation therapy for breast cancer: a longitudinal study.

OBJECTIVE: This longitudinal study aims to examine the present state of perceived control, self-management efficacy, and overall quality of life (QoL) in patients with breast cancer undergoing radiotherapy, and gain insight into the dynamic trends and factors that influence the quality of life experienced by patients during the course of radiotherapy. METHODS: Participants completed the Cancer Experience and Efficacy Scale (CEES), Strategies Used by People to Promote Health (SUPPH), and Functional Assessment of Cancer Therapy- Breast (FACT-B). The data was analyzed using the software SPSS26.0. Repeated measures analysis of variance (ANOVA) and mixed-effects linear models were used to analyze trends in perceived control, self-management efficacy, and QoL at three-time points, as well as factors affecting QoL during radiotherapy. RESULTS: Perceived control and self-management efficacy were associated with QoL over the course of the radiotherapy. Self-management efficacy (ß = 0.30, P < 0.001), presence of chemotherapy (ß = 18.33, P = 0.024), and duration of illness (ß = 2.25, P = 0.028) had a positive effect on the change in QoL, while time (ß = - 2.95, P < 0.001), cancer experience (ß = - 0.46, P < 0.001), and type of medical insurance (ß = - 2.77, P = 0.021) had the negative effect on the change in QoL. CONCLUSION: The QoL, perceived control, and self-efficacy of patients with breast cancer show dynamic changes during radiotherapy. The higher the self-efficacy, the better the QoL, and the worse the QoL when the sense of disease control is poor. At the same time, more attention should be paid to the QoL of breast cancer radiotherapy patients with a long course of the disease, receiving chemotherapy, and different medical payment methods.

Association between self-disclosure and benefit finding of Chinese cancer patients caregivers: the mediation effect of coping styles.

PURPOSE: To examine the relationship between self-disclosure, coping styles, and benefit finding (BF) among caregivers of cancer patients. The study also aimed to identify the factors influencing BF and the impact of coping styles on the relationship between self-disclosure and BF. METHODS: Convenience sampling was used to select 300 caregivers of cancer patients aged greater than 18 years from October 2022 to April 2023 in Chengdu, China. The demographic and clinical characteristics questionnaire, the Benefit Finding Scale (BFS), the Distress Disclosure Index Scale (DDI), and the Simple Coping Style Scale (SCSQ) for caregivers were included in this study. Descriptive statistics, t-tests, one-way analysis of variance, Pearson's correlation analyses, and multiple linear regression models were used. The effect of mediation was tested by the PROCESS macro (Model 4) for SPSS 26.0 by Hayes using 5000 bootstrap samples. RESULTS: There were 292 valid questionnaires (effective response rate 97.33%). The total scores of BF, self-disclosure, negative coping style, and positive coping style of caregivers were 67.77 ± 14.78, 38.23 ± 8.59, 19.68 ± 5.98, and 9.88 ± 4.18, respectively; Pearson's correlation analysis showed that BF was positively correlated with self-disclosure, positive coping, and negatively correlated with negative coping; multiple linear regression analysis showed that self-disclosure, positive coping, and negative coping were influential factors of BF. The results revealed that the effect of self-disclosure on BF was partly mediated by coping styles. It also confirmed that the mediation effect accounted for 54.03% of the total effect. CONCLUSION: The BF of caregivers is at a moderate level. Self-disclosure may influence BF partly because of coping styles.

Comparative analysis of bacterial diversity in two hot springs in Hefei, China.

Hot springs are extreme ecological environments of microbes. The study is the first comparative analysis of bacterial diversity of Tangchi and Bantang hot spring water samples collected in Hefei, China, which is conducive to the further development and utilization of microbial resources in hot springs. Illumina MiSeq system was utilized to sequence and analyze the bacterial 16S rRNA gene from hot spring water samples by bioinformatics, to probe into the bacterial abundance and diversity of two hot springs in Hefei. Results revealed that prevalent bacterial phyla in Tangchi hot spring were Bacillota and Aquificota, and the prevalent bacterial genus was Hydrogenobacter; prevalent phyla in Bantang hot spring were Pseudomonadota followed by Actinobacteriota, and prevalent genera were CL500-29_marine_group and Polynucleobacter. More species and higher evenness in Bantang hot spring than those in Tangchi hot spring. In MetaCyc pathway analysis, the major pathways of metabolism existed in the bacteria from the two hot springs were 'pyruvate fermentation to isobutanol (engineered)', 'acetylene degradation', 'carbon fixation pathways in prokaryotes', 'nitrate reduction I (denitrification)', 'methanogenesis from acetate', 'superpathway of glucose and xylose degradation', etc.

Maresin-2 alleviates allergic airway inflammation in mice by inhibiting the activation of NLRP3 inflammasome, Th2 type immune response and oxidative stress.

Asthma is a chronic inflammatory disease of the respiratory system. Maresin-2 (MaR2) is biosynthesized from docosahexaenoic acid (DHA) by macrophages, display strong anti-inflammatory and pro-resolving activity. To investigate the therapeutic effect and mechanism of MaR2 on asthmatic mice induced by ovalbumin (OVA) in conjunction with the adjuvant aluminum hydroxide. Twenty four female BALB/c mice were randomly divided into control, OVA, OVA + MaR2, and OVA + dexamethasone (Dexa) groups. MaR2 or Dexa were given as a treatment for OVA-induced asthma. Serum, bronchoalveolar alveolar lavage fluid (BALF) and lung tissue were collected for further analysis. The Pathological changes of lung tissue, proportion of inflammatory cells in BALF, levels of inflammatory cytokines in BALF or serum, oxidative stress indices, and the protein concentration of ASC, MPO, Ly-6G, ICAM-1, NLRP3 and Caspase-1 in lung tissues were evaluated. Compared with the OVA group, both OVA + MaR2 and OVA + Dexa group had reduced inflammation and mucus secretion in lung tissue, number of inflammatory cells in BALF, levels of related inflammatory cytokines in serum or BALF, and expressions of ASC, MPO, Ly-6G, ICAM-1, NLRP3 and Caspase-1 proteins in lung tissue. In addition, the oxidative stress was alleviated as indicated by decreased MDA, and elevated SOD and GSH. MaR2 has an obvious protective effect on OVA-induced bronchial asthma in mice, in a similar manner as Dexa. The mechanism may be related to the inhibition of the Th2 type immune response, the NLRP3 inflammasome activation and oxidative stress.

Comparative Analysis of 95 Patients with Different Severity in the Early Outbreak of COVID-19 in Wuhan, China.

OBJECTIVE: To explore the clinical characteristics of patients with different severity in the early outbreak of COVID-19, hoping to provide reference for clinical diagnosis and treatment. METHODS: We retrospectively analyzed the clinical data of 95 COVID-19 patients in Wuhan Red Cross Hospital of China from January 17 to February 13, 2020. All patients were investigated with epidemiological questionnaires. Outcomes were followed up until April 1, 2020. RESULTS: There were 53 males and 42 females, aged 22-84 years (mean 57.3 years). Clinical classification included 54 cases of common type, 27 cases of severe type, and 14 cases of critical type. Six patients had been exposed to the local Huanan seafood market. There were 38 clusters of COVID-19, including 27 family clusters and 11 work unit clusters. Common symptoms included fever (86 (90.5%) of 95), cough (73 (76.8%)), and fatigue (50 (52.6%)). Laboratory findings showed that the most common abnormalities were lymphopenia (75 (78.9%)), elevated D-dimer (60 (63.2%)), and elevated C-reactive protein (56 (58.9%)) on admission. All patients had abnormal chest computed tomography, showing patchy shadows or ground-glass opacities. Severe and critical cases were older, more likely to have shortness of breath, more likely to have underlying comorbidities, and more likely to have abnormal laboratory findings than common cases. The prognosis of patients with different degrees of severity was significantly different. All common and severe patients (100%) were cured and discharged from the hospital, while 10 (71.4%) of 14 critical patients died. CONCLUSIONS: COVID-19 has fast transmission speed and high pathogenicity. We must assess the severity of the disease and take corresponding treatment measures as early as possible.

Diffuse panbronchiolitis: A case report from a Chinese consanguineous marriage family and literature review.

Diffuse panbronchiolitis (DPB) is a chronic diffuse airway inflammatory disease, which is strongly associated with the class I human leukocyte antigen (HLA) alleles. Here, we report a pair of sisters who have been suffering from chronic cough, expectoration and wheezing for many years. They were previously misdiagnosed as chronic bronchitis and bronchial asthma, and were recently diagnosed as diffuse panbronchiolitis. The 36-year-old elder sister suffered from diffuse panbronchiolitis complicated with pulmonary tuberculosis. The 30-year-old younger sister suffered from diffuse panbronchiolitis complicated with bronchial asthma and bronchiectasis. We have performed HLA genotyping research on the two sisters, their parents and younger brother. The results showed that all family members were positive for HLA-A24 and HLA-B13. The younger sister and mother were positive for HLA-A2. The younger brother and father were positive for HLA-A11. We suspect that the two sisters' disease susceptibility may be caused by their parents' consanguineous marriage. In this study, we reported the clinical characteristics of the two sisters with diffuse panbronchiolitis and shared the associated HLA genotyping results of this family cluster, hoping to provide reference for the etiology, diagnosis and treatment of this disease.

Regulation of γδT17 cells by Mycobacterium vaccae through interference with Notch/Jagged1 signaling pathway.

The objective of this study was to investigate the effect of Mycobacterium vaccae on Jagged 1 and gamma delta T17 (γδT17) cells in asthmatic mice. An asthma mouse model was established through immunization with ovalbumin (OVA). Gamma-secretase inhibitor (DAPT) was used to block the Notch signaling pathway. M. vaccae was used to treat asthma, and related indicators were measured. Blocking Notch signaling inhibited the production of γδT17 cells and secretion of cytokine interleukin (IL)-17, which was accompanied by a decrease in Jagged1 mRNA and protein expression in the treated asthma group compared with the untreated asthma group. Similarly, treatment with M. vaccae inhibited Jagged1 expression and γδT17 cell production, which was associated with decreased airway inflammation and reactivity. The Notch signaling pathway may play a role in the pathogenesis of asthma through the induction of Jagged1 receptor. On the other hand, the inhibitory effect of M. vaccae on Jagged1 receptor in γδT17 cells could be used for the prevention and treatment of asthma.

Regulation of γδT17 cells by Mycobacterium vaccae through interference with Notch/Jagged1 signaling pathway

The objective of this study was to investigate the effect of Mycobacterium vaccae on Jagged 1 and gamma delta T17 (γδT17) cells in asthmatic mice. An asthma mouse model was established through immunization with ovalbumin (OVA). Gamma-secretase inhibitor (DAPT) was used to block the Notch signaling pathway. M. vaccae was used to treat asthma, and related indicators were measured. Blocking Notch signaling inhibited the production of γδT17 cells and secretion of cytokine interleukin (IL)-17, which was accompanied by a decrease in Jagged1 mRNA and protein expression in the treated asthma group compared with the untreated asthma group. Similarly, treatment with M. vaccae inhibited Jagged1 expression and γδT17 cell production, which was associated with decreased airway inflammation and reactivity. The Notch signaling pathway may play a role in the pathogenesis of asthma through the induction of Jagged1 receptor. On the other hand, the inhibitory effect of M. vaccae on Jagged1 receptor in γδT17 cells could be used for the prevention and treatment of asthma.

[Effect of hypoxia on the expression and production of fractalkine in pulmonary artery smooth muscle cells and pulmonary microvascular endothelial cells].

OBJECTIVE: To investigate the effect of hypoxia on the expression and production of fractalkine (FKN) in cultured rat pulmonary artery smooth muscle cells (PASMCs) and pulmonary microvascular endothelial cells (PMVECs). METHODS: PASMCs and PMVECs from SD rat were cultured in vitro, and were exposed to hypoxia for 12 h,24 h and 48 h. The expressions of fractalkine mRNA and protein in PASMCs and PMVECs were measured by the methods of in situ hybridization and immunohistochemistry. The fractalkine concentrations in supernatant fluid of cultured PASMCs and PMVECs were measured by enzyme-linked immunosorbent assay. RESULTS: (1) Compared with the control group, the expression and production of fractalkine in PASMCs did not increase after the treatment of hypoxia for 12 hours (P > 0.05), but increased after being treated with hypoxia for 24 hours (P < 0.05), and became more significant after 48 hours (P < 0.01). (2) Compared with the control group, there were no differences of FKN concentrations in supernatant fluid of PMVECs, FKN mRNA and protein levels in PMVECs after being treated with hypoxia for 12 hours, 24 hours or 48 hours (P > 0.05). CONCLUSION: Hypoxia stimulates the synthesis and secretion of fractalkine in cultured rat PASMCs.

Poly[[µ-aqua-bis-(µ-4,4'-bipyridine-κN:N')bis-(µ-3-hy-droxy-adamantane-1-carboxyl-ato-κO:O')bis-(3-hy-droxy-adamantane-1-carboxyl-ato-κO)dicobalt(II)] hepta-hydrate].

The title coordination compound, {[Co(C(11)H(15)O(3))(4)(C(10)H(8)N(2))(2)(H(2)O)]·7H(2)O}(n), consists of a pair of Co(II) atoms, four 3-hy-droxy-adamantane-1-carboxyl-ate anions (L), one water mol-ecule, two bridging 4,4'-bipyridine (4,4'-bpy) ligands and seven uncoordinated water mol-ecules. Both of the Co(II) ions are coordinated in a distorted octa-hedral geometry. Four L ligands bind to each pair of Co(II) atoms in a plane, two of which bridge the two Co(II) atoms as bidentate groups while the other two coordinate to a single Co(II) atom in a monodentate mode. Two half-mol-ecules of 4,4'-bipyridine coordinate the Co(II) atoms from the upside and underside. The packing features extensice O-H⋯O hydrogen bonding.

catena-Poly[[[bis-(3-hy-droxy-adamantane-1-carboxyl-ato-κO)(3-hy-droxy-adamantane-1-carb-oxy-lic acid-κO)zinc(II)]-µ(2)-4,4'-bipyridine] monohydrate].

In the title coordination polymer, {[Zn(C(11)H(15)O(3))(2)(C(10)H(8)N(2))(C(11)H(16)O(3))]·H(2)O}(n), the Zn(II) ion is five coordinated by two N atoms from two 4,4'-bipyridine (4,4'-bpy) mol-ecules and three O atoms from two 3-hy-droxy-adamantane-1-carboxyl-ate anions (L) and one 3-hy-droxy-adamantane-1-carb-oxy-lic acid (HL) mol-ecule. The resulting coordination polyhedron is a near regular ZnN(2)O(3) trigonal bipyramid, with the N atoms in axial sites. The 4,4'-bpy mol-ecules [dihedral angle between the aromatic rings = 17.2 (2)°] act as bridges, connecting the metal ions into an infinite polymeric chain propagating in [[Formula: see text]01]. O-H⋯O hydrogen bonds help to consolidate the packing.

Effects of the TREM-1 pathway modulation during empyema in rats.

BACKGROUND: The activation of triggering receptor expressed on myeloid cells-1 (TREM-1) in the presence of microbial components amplifies the inflammatory response. The aim of the present study was to investigate the effect of the modulation of the TREM-1 pathway during empyema in rats. METHODS: Adult male Wistar rats were subjected to empyema induced by intrapleural injection of Pseudomonas aeruginosa and Staphylococcus aureus. The animals were treated with LP17 (a synthetic TREM-1 inhibitor), a control peptide, or a vehicle (normal saline). Differential cell count, flow cytometry and histological examination were performed to evaluate local inflammatory alterations. Concentrations of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 in both pleural effusion and serum were measured by enzyme-linked immunosorbent assay. RESULTS: Although differential counts of each type of leukocytes in pleural effusion were not affected by LP17, a marked reduction in neutrophil numbers was seen in LP17 treated rats due to the reduction of both pleural effusion volume and total cell numbers. LP17 administration impaired concentration elevation in tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 in both pleural effusion and serum. It was found that survival rate in LP17 treated rats was much higher than that in control rats. CONCLUSION: The modulation of the TREM-1 pathway by the use of LP17 appears to be beneficial during empyema in rats in attenuating pleural and systemic inflammatory responses.

[Effect of fractalkine on proliferation of pulmonary artery smooth muscle cells].

AIM: To investigate the effect of fractalkine on cell proliferation of cultured rat pulmonary artery smooth muscle cells (PASMCs) in vitro. METHODS: Rat PASMCs were cultured in vitro, and treated with different concentrations (10(-10), 10(-9), 10(-8) mol/L) of fractalkine for 12 h, 24 h and 48 h. The cell proliferation was quantified by MTT assay. The cell cycle of PASMCs was measured by flow cytometric(FCM) analysis. RESULTS: MTT assay showed that fractalkine promoted significantly the proliferation of PASMCs, and the effect was concentration-dependent. FCM analysis indicated that fractalkine increased the percentage of S phase and proliferative index (PI). The percentage of S phase and PI of PASMCs were increased after treated with fractalkine for 12 hours, which reached a maximal level at 24 hours. CONCLUSION: Fractalkine promotes rat PASMCs proliferation in a concentration-dependent manner.

[The change of fractalkine in lung tissue of rat with hypoxic pulmonary hypertension].

OBJECTIVE: To evaluate the role of fractalkine in the pathogenesis of hypoxic pulmonary hypertension. METHODS: Twenty male SD rats were randomly divided into control group and hypoxic group. Rats in hypoxic group were exposed to hypoxia for 3 weeks. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization. The thickness of pulmonary arterioles was measured with a computerized image analyzer. The rates of wall thickness/external diameter (WT%) and wall area/total vascular area (WA%) were calculated. The fractalkine level in lung tissue were measured by enzyme-linked immunosorbent assay. Fractalkine mRNA expression in lung were observed by reverse transcriptase-polymerase chain reaction. RESULTS: The rat mPAP of hypoxic group was higher than that of the control group [(28.7 +/- 3.8) mmHg vs (16.3 +/- 2.1) mmHg, P < 0.01]. The WT% and WA% were increased significantly in hypoxic group than in control group (WT%: (21.28 +/- 4.60)% vs (10.20 +/- 1.56)%, WA%: (67.08 +/- 9.44)% vs (38.11 +/- 42.30)%, P < 0.01, respectively]. In hypoxic group, the expression of fractalkine mRNA in the lung was significantly up-regulated [(0.49 +/- 0.05) vs (0.29 +/- 0.02), P < 0.01], the expression level of fractalkine in lung tissue was higher than that in control group [(7622.6 +/- 938.4) pg/mL vs (4168.5 +/- 403.5) pg/mL, P < 0.01. Linear correlation analyses showed that fractalkine mRNA and protein were positively associated with WA% and WT% (P < 0.05). CONCLUSION: The synthesis and release of fractalkine are increase in the lung tissue of chronic hypoxic rats, and fractalkine may play an important role in hypoxic pulmonary hypertension.

[Effect of simvastatin on endothelin-1 expression in endothelial cell cultured hypoxically].

OBJECTIVE: To observe the role of simvasatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, in synthesis and excretion of endothelin-1 (ET-1) in endothelial cell cultured hypoxically. METHODS: Human umbilical vein endothelial cells were hypoxically cultured and treated with simvastatin by different concentrations (0, 1.0, 2.5, 5.0, 10.0 micromol/L) and different times (12, 24, 48 h). Mevalonate was used to intervent the effect of simvastatin. Reverse transcription-polymerase chain reaction (RT-PCR)and enzyme-linked immunoadsorbent assay (ELISA) were adopted to measure ET-1 mRNA and ET-1 in supernatant fluid of endothelial cell culture. RESULTS: (1) There were no changes of ET-1 mRNA and ET-1 expression after the hypoxically cultured endothelial cell were incubated with 1 MICROmol/L simvastatin, but ET-1 expression decreased without significant difference compared to control (0 micromol/L simvastatin) when interfered with 2.5 micromol/L simvastatin. The decreases of ET-1 mRNA and ET-1 expression became more obvious when expression were interfered by 5 micromol/Land 10 micromol/L simvastatin (P < 0.01). (2) ET-1 mRNA and ET-1 expression decreased at 12 h after the endothelial cells were incubated with 10 micromol/L simvastatin, which became more fewer at 24 h and reached the minimum expression at 48 h (P < 0.01). (3) The inhibition effect of simvastatin on ET-1 mRNA and ET-1 expression of endothelial cells could be prevented by mevalonate with concentration of 100 micromol/L. CONCLUSION: Simvastatin can inhibit ET-1 expression in endothelial cell cultured hypoxically.

[The change of fractalkine in serum and pulmonary arterioles of hypoxic rat].

OBJECTIVE: In order to evaluate the role of fractalkine in the pathogenesis of hypoxic pulmonary hypertension, we observed the change of serum soluble fractalkine and the expression of fractalkine in pulmonary arterioles of rat at different phase of hypoxia-induced pulmonary hypertension development. METHODS: The rat model of hypoxic pulmonary hypertension was duplicated by intermittent hypoxia. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization. The thickness of pulmonary arterioles was measured with a computerized image analyzer. Serum soluble fractalkine concentrations were measured by enzyme-linked immunosorbent assay. The expressions of fractalkine mRNA and protein in pulmonary arterioles were detected by in situ hybridization and immunohistochemical analysis, respectively. RESULTS: Compared to control, the mPAP of rats was markedly elevated after hypoxia for 14 days (P < 0.01), but the index of wall thickness of pulmonary arterioles (WT% and WA%) and the index of right ventricular hypertrophy CRV/(LV+S)] increased significantly at 21 days of hypoxia (P < 0.01). In rats exposed to hypoxia for 21 days, the fractalkine mRNA and protein levels in pulmonary arterioles were up-regulated significantly (P < 0.01), and the serum soluble fractalkine concentrations were also elevated (P < 0.01), as compared with control. Linear correlation analysis showed that the fractalkine mRNA level in pulmonary arterioles was associated with WA% (r = 0.749, P < 0.01) and WT% (r = 0.732, P < 0.01), the fractalkine protein level in pulmonary arterioles was also correlated with WA% (r = 0.727, P < 0.01) and WT% (r = 0.683, P < 0.01). CONCLUSION: The chronic hypoxia stimulates the synthesis and release of fractalkine. Fractalkine plays an important role in regulating the pulmonary vascular remodeling.

[Research on Rho-kinase expression in pulmonary arterioles of rat exposed to hypoxia].

OBJECTIVE: To evaluate the expression and the role of Rho-kinase (ROCK I and ROCK II )in the development of hypoxic pulmonary hypertension of rat. METHODS: Thirty six of adult male SD rats were randomly divided into six groups; one group was exposed to air as normal control, the other five groups were exposed to isobaric hypoxia for 1 day, 3 days, 1 week, 2 weeks and 3 weeks respectively. Microtube method was used to measure the mean pulmonary arterial pressure (mPAP). The right ventricle (RV) and left ventricle plus atrial ventricular septum (LV+S) were isolated and weighed to calculate the value of RV/(LV+S). The amounts of Rho-kinase and Rho-kinase mRNA in rat pulmonary artery were determined by immunohistochemistry, in situ hybridization and image analysis. RESULTS: The mPAP and RV/(LV+S) values increased with time prolongation of rats exposed to hypoxia (P<0.05). The ratio of arteriole wall thickness/vascular external diameter(WT%) and vascular area/total vascular area(WA%) went forward to a height with exposing rats to hypoxia for a long time; WT% and WA% of hypoxia group rats exposed for 3 weeks were significantly higher than that of control group (P<0.05). All of ROCK I , ROCK II, ROCK I mRNA and ROCK II mRNA in pulmonary arterioles got the enhanced positive signals of immunohistochemistry staining or in situ hybridization with prolonging the time of rats exposed to hypoxia. The hypoxia group for 3 weeks got significantly stronger staining signals of Rho-kinase and Rho-kinase mRNA in pulmonary arterioles than that of control group (P<0.05). The positive staining of ROCK I , ROCK I mRNA, ROCK II or ROCK II mRNA in pulmonary arterioles all positively related with mPAP, WA% and WT% (r=0.404, 0.267 and 0.263; 0.500, 0.263 and 0.260; 0.490, 0.295 and 0.286; 0.579, 0.251 and 0.254) (P<0.05). CONCLUSIONS: Hypoxia led Rho-kinase and Rho-kinase mRNA to have an increased expression. Rho-kinase may play a role in the development of hypoxic pulmonary hypertension by contracting and remodeling pulmonary arterioles.

[Preventive effects of montelukast on the collagen expression of pulmonary arterioles in rats with chronic hypoxia].

OBJECTIVE: To evaluate the preventive effects of montelukast on the collagen expression of pulmonary arterioles in chronic hypoxic rats. METHODS: Thirty male Wistar rats were randomly divided into three groups: control group, hypoxic group and montelukast preventive group. The animal model of pulmonary hypertension was established by exposing the rats to normabaric hypoxic conditions 8 hours q.d. for 3 weeks. The expression levels of collagen I and III in arterioles were observed by immunohistochemistry. RESULTS: The positive degree of collagen I in pulmonary arterioles of hypoxic group was higher than that of control group (1.51+/-0.09 vs 1.15+/-0.05, P<0.01), and the positive degree of collagen I in pulmonary arterioles of preventive group (1.19+/-0.06) was lower than that of hypoxic group (P<0.01). The differences of positive degree of collagen III in pulmonary arterioles were not significant among the three groups (P>0.05). CONCLUSION: Montelukast can reduce the hypoxia-induced deposition of collagen I in the pulmonary arterioles wall.

[The effects of losartan on pulmonary arterial collagen and AT1 in chronic hypoxic rats].

OBJECTIVE: To investigate the effects of losartan on pulmonary arterial collagen and AT1 in chronic hypoxic rats. METHODS: Thirty male SD rats were randomly divided into three groups: control group, hypoxic group and therapeutic group. The animal model of pulmonary hypertension was established by exposing the rats to normabaric hypoxic conditions for three weeks. Then, the therapeutic group was given losartan for two weeks. We measured the expression of Collagen I, III and AT1 in arterioles by means of immunohistochemistry. RESULTS: The positive degree of Collagen I in pulmonary arterioles in the hypoxic group was higher than that in the control group [(1.5202+/-0.069) vs (1.1324+/-0.071), P<0.01]; but in the therapeutic group it was lower than that in the hypoxic group [(1.1637+/-0.062) vs (1.5202+/-0.069), P<0.01]. There was no significant difference in collagen III and AT1 among the three groups (P>0.05). CONCLUSION: Losartan could reduce pulmonary arterial collagen I expression, it may be one of the therapeutic mechanisms on hypoxic pulmonary hypertension of losartan.