[Effect of triptolide on the expression of RANTES in the renal tissue of diabetic nephropathy rats].

OBJECTIVE: To investigate the effect of triptolide (TPL) on the renal tissue of diabetic rats and its possible mechanisms. METHODS: SD rats were randomly divided into the normal control group (as the normal group), the diabetic model group (the model group), the low dose TPL treatment group (the low dose TPL group, TPL 0.2 mg/kg by gastrogavage), the high dose TPL treatment group (the high dose TPL group, TPL 0.4 mg/kg by gastrogavage). Equal volume of normal saline was given to rats in the normal group and the model group. Five rats were randomly selected from each group at week 4, 8, and 12 of the experiment to detect body weight, kidney weight, 24 h urinary albumin (24 h UAL), plasma glucose (FBG), total cholesterol (TC), total triglyeride (TG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), white blood cell (WBC), and hemoglobin A1c (HbA1c). The mRNA and protein expression of regulated upon activation normal T-cell expressed and secreted (RANTES) in the renal tissue was assessed by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA). The renal tissue was pathologically stained by HE, PAS, and Masson staining. The glomerular and renal tubular interstitial lesions were observed at each time point. The glomerular sclerosis index (GSI) was observed by PAS staining, and the renal interstitial filrosis index (RIFI) was calcutated. RESULTS: Compared with the same group at week 4, the expression of 24 h UAL, RANTES, GSI, and RIFI at week 12 significantly decreased in two TPL groups (P <0.01). Compared with the same group at week 8, the expression of 24 h UAL, RANTES, GSI, and RIFI at week 12 also significantly decreased in the two TPL groups (P <0. 05, P <0.01). Compared with the normal group, body weight and the kidney weight obviously decreased at week 4, 8, and 12 in the model group (P <0. 01); 24 h UAL, FBG, TG, TC, HbA1c, RANTES, GSI, and RIFI were obviously elevated (P <0.01). Compared with the model group, 24 h UAL, RANTES, GSI, and RIFI also decreased in the two TPL treatment groups (P <0.01). Compared with the low dose TPL group, they were attenuated in the high dose TPL group (P <0. 05, P <0. 01). CONCLUSION: TPL could not only inhibit the over-expression of RANTES, but also improve the glomerular sclerosis and renal interstitial fibrosis in the renal tissue of diabetic rats.

Influence of auricular plaster therapy on sleeping structure in OSAS patients.

OBJECTIVE: To evaluate the therapeutic effects of auricular plaster therapy for obstructive sleep apnea syndrome (OSAS) and the influence on sleeping structure. METHODS: 45 OSAS patients were randomly divided into a treatment group of 30 cases and a control group of 15 cases for comparison of the changes in parameters of respiration and sleep at night. RESULTS: The auricular plaster therapy significantly improved the hypoventilation index, respiratory disturbance index and other respiratory parameters as well as the sleeping parameters such as the time and rate of sleep at stage I and II, and the waking time and rate. CONCLUSION: Auricular plaster therapy may show good therapeutic effects for OSAS, and with the advantages of low cost and less side effects.

[The change and significance of coagulation activity in bleomycin-induced lung fibrosis in rats].

OBJECTIVE: To investigate the role of coagulation activity of bronchoalveolar lavage fluid (BALF) in the pathogenesis of lung fibrosis. METHODS: Fourty-eight Sprague-Dawley rats were randomly divided into 2 groups, 24 rats in each group. In the bleomycin (BLM) group, the lung fibrosis model was made by tracheal instillation of bleomycin A(5) (BLMA(5), 5 mg/kg). At day 7, 14, 28 and 40, the recalcification time of normal pooled plasma, factor VII and X deficiency plasma were measured for procoagulation activity (PCA), and the thrombin activity and the protein level of transforming growth factor beta(1) (TGF-beta(1)) in BALF were also measured. In the control group, normal solution was instillated into the lungs. RESULTS: In the BLM group, the recalcification time of normal pooled plasma in BALF at the four time points were (56 +/- 10), (78 +/- 4), (172 +/- 11) and (180 +/- 6) s respectively, while in the control group, were (190 +/- 10), (186 +/- 8), (184 +/- 6) and (185 +/- 6) s respectively. The thrombin activity at the four time points were (1.26 +/- 0.03), (0.82 +/- 0.05), (0.28 +/- 0.03) and (0.28 +/- 0.02) microg/ml respectively in the BLM group, but were (0.31 +/- 0.02), (0.32 +/- 0.03), (0.31 +/- 0.04) and (0.29 +/- 0.05) microg/ml respectively in the control group. The level of TGF-beta(1) at the four time points were (310 +/- 36), (220 +/- 30), (109 +/- 12) and (96 +/- 11) ng/ml respectively in the BLM group, but were (92 +/- 20), (94 +/- 12), (92 +/- 10) and (90 +/- 9) ng/ml respectively in the control group. The above measurements were significantly different in day 7 and 14 between the BLM group and the control group (P < 0.01), while the differences were not significant at day 28 and 40 (P > 0.01). In the BLM group, at day 7 and 14, the recalcification time of factor VII deficiency plasma was (123 +/- 12) and (162 +/- 4) s respectively; the recalcification time of factor X deficiency plasma was (357 +/- 22) and (387 +/- 12) s respectively; the recalcification time of factor X deficiency plasma was longer than that of factor VII deficiency plasma and that of normal pooled plasma. Within 14 day, the level of TGF-beta(1) was positively correlated with PCA and thrombin activity. CONCLUSIONS: During the period of alveolitis, the PCA and thrombin activity were upregulated in BALF, which was caused by activated factor VII activating factor X and the switching to the exogenous coagulation pathway. But during the period of lung fibrosis, their activities were not upregulated. These results suggest that the coagulation factor and thrombin might contribute to the development of pulmonary fibrosis by promoting production of TGF-beta(1).

[The change and significance of the cardiopulmonary exercise test parameters in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To investigate the change of exercise cardiopulmonary function in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Thirty OSAHS patients and 18 normal healthy adults (control group) were studied by cardiopulmonary exercise test (CPET). The results including maximal oxygen uptake percent predicted (Vo(2)max% predicted), oxygen uptake to work rate (Vo(2)/WR), oxygen pulse percent predicted (Vo(2)/HRmax% predicted), anaerobic threshold to maximal oxygen uptake (AT/Vo(2)max), breathing reserve (V(E)max/MVV) and ventilatory equivalents for carbon dioxide (V(E)/V(CO2)) were compared between two groups. RESULTS: The levels of Vo(2)max% predicted, AT/Vo(2)max, Vo(2)/HRmax% predicted, Vo(2)/WR, and V(E)max/MVV in the OSAHS group [(83 +/- 5)%, (44 +/- 6)%, (79 +/- 5)%, (9.3 +/- 0.6) ml.min(-1).W(-1), (73 +/- 8)%] were lower than those in the control group [(88 +/- 5)%, (49 +/- 6)%, (83 +/- 4)%, (10.9 +/- 2.3) ml.min(-1).W(-1), (79 +/- 9)%, all P < 0.05]. The levels of V(E)/V(CO2) in the OSAHS group (29 +/- 3) was higher than the control group (26 +/- 3, P < 0.05). In the OSAHS group Vo(2)max% predicted, Vo(2)/HRmax% predicted, Vo(2)/WR AT/Vo(2)max and V(E)max/MVV correlated negatively with apnea-hypopnea index (AHI, r = -0.52, -0.62, -0.59, -0.37, -0.66, P < 0.05). Vo(2)max% predicted, Vo(2)/HRmax% predicted, Vo(2)/WR, AT/Vo(2)max and V(E)max/MVV correlated with lowest oxygen saturation (LSaO(2), r = 0.60, 0.63, 0.64, 0.40, 0.59, P < 0.05). V(E)/V(CO2) correlated with AHI (r = 0.57, P < 0.01) and correlated negatively with LSaO(2) (r = -0.62, P < 0.01). CONCLUSIONS: The cardiac output of patients with OSAHS can not meet the demand of hard exercise. At the same time, there is more significant ventilation-perfusion disturbance in OSAHS patients than normal subjects. The patients' exercise cardiopulmonary function has been compromised although there are no symptoms.

[Clinical observation on effect of auricular acupoint pressing in treating sleep apnea syndrome].

OBJECTIVE: To study the clinical effect and mechanism of auricular acupoint pressing (AAP) in treating sleep apnea syndrome (SAS). METHODS: Forty-five patients with SAS were randomly divided in to the AAP group (30 patients) and the control group (15 patients) to observe the changes of clinical symptoms, apnea-hypopnea index (AHI), apnea index (AI), hypopnea index (HI) and minimum blood oxygen saturation (mSaO2) in night before and after treatment by multiple channel polysomnography (PSG). RESULTS: Clinical symptoms were significantly alleviated in the AAP group after treatment, with improvement in various parameters monitored by PSG (P < 0.01), showing significantly reduced AHI, AI and HI and increased mSaO2 (P < 0.01). While in the control group, no improvement was found either in clinical symptom or in PSG parameters (P > 0.05). Comparison between the two groups showed significant difference (P < 0.01). CONCLUSION: AAP is an effective treatment of SAS, it provides a facilitate, economic and safe therapy for early prevention and treatment to SAS.

[Changes of the platelet function and serum anticardiolipin antibody in patients with pulmonary thromboembolism].

OBJECTIVE: To explore the changes of the platelet function and serum anticardiolipin antibody (ACA) in patients with pulmonary thromboembolism (PTE). METHODS: Forty-eight patients with PTE diagnosed by spiral computed tomographic pulmonary angiography (CTPA) were included as the trial group, while 20 person in which PTE was excluded served as the control group. P-selectin, and GPIIb/IIIa expressed on platelets were measured by flow cytometry, and plasma TXB(2), 6-Keto-PGF1alpha, vWF, D-dimer and serum ACA were measured by ELISA and the changes of these parameters were compared 1 week later. RESULTS: In the trial group, the levels of P-selectin, GPIIb/IIIa, TXB(2), vWF, D-dimer and T/K were significantly higher than those in the control group (P < 0.01). But the plasma level of 6-Keto-PGF1alpha in the patients with PTE was significantly lower than that in the control group (P < 0.01). The levels of ACA-IgG and ACA-IgA were significantly higher than those in the control group (P < 0.01). After therapy the level of 6-Keto-PGF1alpha was significantly higher than that before therapy (P < 0.01), and other parameters were significantly lower than those before therapy (P < 0.01). P-selectin, GPIIb/IIIa and vWF were positively correlated with D-dimer (P < 0.01). CONCLUSION: Endothelium damage, platelet activation and hypercoagulation combined with fibrinolytic activation occur in patients with PTE.

[Detection of thromboxane B2, 6-keto-prostaglandin F1alpha and anticardiolipin antibody in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To observe the changes of thromboxane B(2) (TXB(2)), 6-keto-prostaglandin F1alpha (6-K-PGF1alpha) and anticardiolipin antibody (ACA) in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) before and after institution of nasal continuous positive airway pressure (nCPAP). METHODS: Sixty cases of OSAHS confirmed by polysomnography (PSG) were selected as the trial group, and 20 normal donors without OSAHS were recruited as the control group. Nineteen patients with severe OSAHS were treated by nCPAP. Plasma levels of TXB(2), 6-K-PGF1alpha were detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: Plasma (serum) level of TXB(2) (ACA) was significantly higher in patients with moderate to severe OSAHS than that in control group (P < 0.01), and nCPAP therapy decreased its level significantly (P < 0.01). Plasma level of 6-K-PGF1alpha was significantly lower than that in the control group (P < 0.01), and nCPAP therapy increased its level significantly (P < 0.01). TXB(2) and ACA were correlated positively with AHI, and negatively with minimal oxygen saturation (P < 0.01). 6-K-PGF1alpha was correlated negatively with AHI, and positively with minimal oxygen saturation (P < 0.01). CONCLUSIONS: The results indicate that patients with OSAHS are susceptible to thromboembolism disease. TXB(2), 6-K-PGF1alpha, ACA may be associated with the high prevalence of thromboembolism in patients with OSAHS. nCPAP therapy is effective in correcting TXB(2), 6-K-PGF1alpha, ACA.