We treated two cases of flaccidity syndrome,one who was suffering obstinate myasthenia gravis was treated by modified Mahuang Fuzi Xixin decoction which is based on warming Yang and replenishing qi,dredging the meridian passage.The other who was suffering lipid storage myopathy was treated by modified Buzhong Yiqi decoction which is based on strengthening spleen and improving digest,ascending the clear and descending the turbid,supplementing qi and nourishing blood, promoting blood circulation to remove meridian obstruction.Both got the obvious improvement.

Hepatolenticular degeneration,namely Wilson's disease,an autosomal recessive disorder of copper metabolism.The author of this article gave a definition to toxin-pathogen,discussed the basic concept of collaterals disease briefly.And pointed out that hepatolenticular degeneration is a disease due to toxin-pathogen invading collaterals,which was caused by disorder of copper metabolism.This can result in toxin stagnating in collaterals and stagnation of blood stasis in collaterals in the initial stage,and collaterals injured at last.To improve QI-blood circulation and regulate the function of zang fu is important in order to accelerate elimination of toxin and prevent copper from stagnating. Specific therapy vary according to different clinical symptoms,such as promoting blood circulation for removing obstruction in collaterals and clearing toxin, clearing heat-fire and clearing toxin and dispersing stagnated liver-qi for promoting bile flow et al.

Objective To explore the role of oxygen free radicals in the proliferation of ECV304 induced by AngⅡ.Methods The lines of human umbilical vein endothelial cell(ECV304)cultured in vivo were divided into three groups which were treated by AngⅡ,AngⅡ+N-acetyl-L-cysteine(NAC),and normal culture medium.First we observed the proliferous effect of ECV304 induced by AngⅡat different concentration with improved MTT and microscope.Then the contents of oxygen free radicals(?OH)in three groups were detected by spectrophotometer.Results ECV304 incubated with AngⅡ(0.03125～1?mol/L)for 12 hours increased the proliferation rate(P 0.05 vs.control group).Conclusions ECV304 induced by AngⅡcan produce oxygen free radicals(?OH),and the contents of oxygen free radicals(?OH) increase with the prolongation of time and the enlargement of dose;Antioxidant NAC can inhibit the proliferation of ECV304 induced by AngⅡ,this effect may be related with reducing the content of oxygen free radicals(?OH);oxygen free radicals(?OH)may be one of the major mocleculars which play an important role in the signal transduction of ECV304 proliferation.

AIM: To investigate the urinary protein (UP) excretion in rats suffering from renal ischemia-reperfusion (I-R) and effect of nitric oxide on it. METHODS: SD rats were used to establish the renal I-R model. Sodium nitroprusside (SNP), N ?-nitro-L-arginine (L-NNA) and aminoguanidine (AG) were used to determine the effect of nitric oxide on UP excretion under renal I-R. Quantitative analysis of UP was made by chromatometry. UP species were separated by SDS-PAGE. RESULTS: Renal I-R caused significant increase in UP ( P

Objective To investigate the anti-fibrotic effect of Kudancao tablets on bleomycin-induced pulmonary fibrosis in rats . Methods Forty healthy adult SD rats(200±20g)were randomly divided into 4 groups: normal control group(without any treatment),normal saline group(intratracheal instillation of normal saline), model group(intratracheal instillation of 5mg/kg of Bleomycin)and kudancao tablets group(intragastric administration of kudancao tablets suspended in normal saline,0.705g/(100 g.d),2 times/day and for 5 times, then intratracheal instillation of 5 mg/kg of Bleomycin 1h later). Rats in all groups were scraficed 14d and 28d after intratracheal instillation. Alkali hydrolysis method was used to detect the HYP content in lung tissues. The pathological changes were observed with HE staining and silver staining. ResultsCompared with the normal control group and normal saline group,the HYP content in the lung tissues of rats in model group increased significantly (P<0.01). Compared with the model group,the HYP content in the lung tissues of rats in kudancao tablets group decreased significantly(P<0.01). Pathological examination showed that significant fibrotic changes were found in lungs of rats in model group,while the fibrotic changes were ameliorated in lungs of rats in kudancao tablets group. ConclusionKudancao tablets may decrease the hydroxyproline content in lung tissues,and ameliorate the fibrotic degree of lungs of rats with bleomycin-induced pulmonary fibrosis.

AIM To investigate the expression of pep-tide transporter (PEPT)2 mRNA in the lungs of ratswith lipopolysaccharide(LPS)-induced acute lung inju-ry. METHODS Health male Sprague-Dawley rats were divided randomly into 5 groups: normal control,cheally) given groups. Lung histopathological changes were observed under light microscope. Lung wet-to-dry weight (W/D) ratios, total protein concentration in bronchoalveolar lavage fluid (BALF) and lung my-eloperoxidase(MPO) activity were measured. The ex-pression levels of PEPT2 mRNA were evaluated by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS Typical pathological inflammation changes in the lungs, including alveolar congestion, hemorrhage, edema, infiltration of neutro-phils in the air space or vessel wall, thickness of the alveolar wall, and hyaline membrane formation, were observed in LPS groups. The lung W/D ratios in LPS 2, 4 and 8 h groups (4.72±0.18, 5.06±0. 17 and 5.12±0.16) were significantly higher than those innormal control and saline groups (4.12±0. 15 and 4.14±0.11). Compared with normal control and sa-g-1 wet tissue], MPO activity increased obviously in LPS2,4 and 8 h groups[(1.96±0.15), (2.23±protein concentration in BALF in LPS 2, 4 and 8 hgroups [ (36.6±2.9), ( 86.9±3.5 ) and (92.2±There was no statistical difference in PEPT2 mRNA levels in the lungs of rats among all groups. CON-CLUSION PEPT2 mRNA level does not change sig-nificantly in the acute injured lung tissue induced by LPS.

Objective To investigate the role of ischemic postconditioning(I-post) on intestinal mucosa in rats with ischemia-reperfusion (I/R) injury.Methods By using rat model of intestine I/R injury,32 male Sprague-Dawley rats were randomly divided into 4 groups: sham-operation group(S),I/R group(I/R),ischemic preconditioning group(IPC),and ischemic postconditioning group(I-post),respectively.The contents of malondialdehyde(MDA), the activity of superoxidase dismutase(SOD),and the activity of myeloperoxidase(MPO) in intestinal mucosa were measured respectively.The status of intestinal mucosa cellular apoptosis was detected by TdT-mediated dUTP-biotin nick end labeling(TUNEL).Chiu's count was used to assess the changes in intestinal pathological morphology.Results The content of MDA and activity of MPO were significantly reduced and the activity of SOD was enhanced in IPC group and I-post group compared with I/R group.There was obvious cellular apoptosis after reperfusion,and the apoptotic index in I-post group and IPC group was significantly lower than that in I/R group.Conclusion Ischemic postconditioning can result in protection against intestinal mucosa with I/R injury,which may be related to reducing the production of oxygen free radicals,maintaining the activities of antioxidant systems,and reducing intestinal mucosa cellular apoptosis.

Objective To investigate the effects of ischemic postconditioning (I-post) on intestinal mucosa mitochondrion after ischemia-reperfusion (IR) injury in rat intestine.Methods By using rat model of intestine IR injury,male Sprague-Dawley rats were divided into 4 groups:sham-operation group (S),IR group (IR),ischemic preconditioning group (IPC),and I-post group.Intestinal mucosa mitochondrial ultrastructural changes were observed by using transmission electron microscope (TEM).Mucosal cellular mitochondrial respiration function was studied by measuring the mitochondrial dehydrogenase-dependent reduction of MTT to its formazan derivative,and intestinal mucosal mitochondrial membrane potential was detected by confocal laser scanning microscopy.Results Compared with that in IR group,the injury of mitochondrion in I-post group and IPC group began to recover.The mitochondrial respiratory function and the mitochondrial membrane potential were significantly improved in I-post group and IPC group (P0.05).Conclusion The mechanism of ischemic postconditioning against IR injury of intestine in rats is partly related to maintaining the mitochondrial ultrastructural changes and respiratory function and improving mitochondrial membrane potential.

AIM: To study the role of polymorphonuclear neutrophile(PMN) in lipopolysaccharide (LPS)- induced acute lung injury (ALI) and the protective effect of interleukin - 10(IL - 10) on ALI. METHODS: LPS alone (100 ?g) or LPS+ IL-10 (l ug) was instilled intratracheally into rats. PMN numbers, protein content and malondialdehyde (MDA) content in bronchoalveolar lavage fluid (BALF) were measured. Histological change of lung was also observed. RESULTS: LPS increased significantly PMN numbers, protein content and MDA content in BALF. Histological finding shows PMN accumulation in lung. IL - 10+LPS reduced remarkably PMN numbers ,pro- tein content and MDA content in BALF than those caused by LPS. PMN decreasing was also identified by light microscopy. CONCLUSION: LPS instilled intratracheally causes PMN accumulation in lung and ALI, while IL - 10 could alleviate ALI through reducing PMN accumulation.

AIM and METHODS: The animal model of acute lung injury (ALI) caused by intratracheal instillation of lipopolysaccharides(LPS) in vivo and human peripheral blood polymorphonuclear neutrophil (PMN) in vitro were used to study the effects of sodium nitroprusside (SNP), nitric oxide (NO) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. RESULTS: ① In vivo , PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye and monastral blue dye extravasation in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS+SNP group. ② In vitro, the apoptotic percentage of SNP group was much higher than that of control group, while compared with LPS group, SNP+LPS group has significantly higher apoptotic percentage. CONCLUSIONS: SNP intratracheal instillation attenuated LPS-induced microvascular permeability and alleviated ALI. PMN apoptosis induced by SNP may be one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.