A new bibenzyl derivative from stems of Dendrobium officinale / 中国中药杂志

Eleven compounds were isolated from the 95% ethanol extract of the stems of Dendrobium officinale after water extraction by various modern chromatographic techniques, such as silica gel column chromatography(CC), octadecyl-silica(ODS) CC, Sephadex LH-20 CC, preparative thin layer chromatography(PTLC) and preparative high performance liquid chromatography(PHPLC). According to spectroscopic analyses(MS, 1D-NMR, 2D-NMR) combined with optical rotation data and calculated electronic circular dichroism(ECD), their structures were identified as dendrocandin Y(1), 4,4'-dihydroxybibenzyl(2), 3-hydroxy-4',5-dimethoxybibenzyl(3), 3,3'-dihydroxy-5-methoxybibenzyl(4), 3-hydroxy-3',4',5-trimethoxybibenzyl(5), crepidatin(6), alternariol(7), 4-hydroxy-3-methoxypropiophenone(8), 3-hydroxy-4,5-dimethoxypropiophenone(9), auriculatum A(10) and hyperalcohol(11). Among them, compound 1 was a new bibenzyl derivative; compounds 2 and 7-11 have not been previously reported from Dendrobium plants; compound 6 was reported from D.officinale for the first time. Compounds 3-6 exhibited potent antioxidant activity with IC_(50) values of 3.11-9.05 μmol·L~(-1) in ABTS radical scavenging assay. Compound 4 showed significant inhibitory effect on α-glucosidase, with IC_(50) value of 17.42 μmol·L~(-1), indicating that it boasted hypoglycemic activity.

Clinical observation on tuina plus Baixiao moxibustion for temporomandibular joint dysfunction syndrome / 针灸推拿医学（英文版）

Objective:To observe the clinical effect of tuina plus Baixiao moxibustion in the treatment of temporomandibular joint dysfunction syndrome (TJDS). Methods: A total of 70 TJDS patients who met the inclusion criteria were randomized into an observation group and a control group by flipping a coin, with 35 cases in each group. Patients in the observation group were treated with tuina plus Baixiao moxibustion, while patients in the control group received oral intake of diclofenac potassium (75 mg/pill), 1 pill after every dinner. Both tuina and Baixiao moxibustion were done once a day during treatment. The therapeutic evaluation was evaluated after 10 treatments in both groups. The maximum mouth opening distance and visual analog scale (VAS) were observed before and after treatment, and the therapeutic efficacy was also compared. Results: After treatment, the maximum mouth opening distance and VAS improved in both groups (all P＜0.05); both items in the observation group were superior to those in the control group (both P＜00.05). The total effective rate was 91.4% in the observation group, versus 74.3% in the control group, and the between-group comparison of the total effective rate showed statistical significance (P＜0.05). Conclusion: Tuina plus Baixiao moxibustion can effectively improve TJDS patient’s temporomandibular joint function and alleviate pain, with better efficacy than oral intake of diclofenac potassium.

Effects of Nerve Growth Factor on Cardiac Fibroblasts Proliferation, Cell Cycle, Migration, and Myofibroblast Transformation / 中华医学杂志(英文版)

<p><b>Background</b>Recent research indicates that nerve growth factor (NGF) promotes cardiac repair following myocardial infarction by promoting angiogenesis and cardiomyocyte survival. The purpose of this study was to investigate the effects of NGF on cardiac fibroblasts (CFs) proliferation, cell cycle, migration, and myofibroblast transformation in vitro.</p><p><b>Methods</b>CFs were obtained from ventricles of neonatal Sprague-Dawley rats and incubated with various concentrations of NGF (0, 0.01, 0.1, 1, 10, and 100 ng/ml; 0 ng/ml was designated as the control group). Cell proliferation and cell cycle of the CFs were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry (FCM), respectively. A cell scratch wound model and transwell were carried out to observe effects of NGF on migration of CFs after 24 h of culture. Real-time polymerase chain reaction (RT-PCR) and Western blotting were used to measure α-smooth muscle actin (α-SMA) at mRNA and protein levels after CFs were incubated with various concentrations of NGF.</p><p><b>Results</b>Expression of α-SMA measured by RT-PCR and Western blotting significantly increased in the 1 and 10 ng/ml NGF groups (P < 0.05). Absorbance values of CFs showed that NGF did not influence the proliferation of CFs (The Avalues were 0.178 ± 0.038, 0.182 ± 0.011, 0.189 ± 0.005, 0.178 ± 0.010, 0.185 ± 0.025, and 0.177 ± 0.033, respectively, in the 0, 0.01, 0.1, 1, 10, and 100 ng/ml NGF groups [P = 0.800, 0.428, 0.981, 0.596, and 0.913, respectively, compared with control group]), and FCM analysis showed that the percentage of CFs in G0/G1, S, and G2/M phases was not changed (P > 0.05). The cell scratch wound model and transwell showed that CFs migration was not significantly different (P > 0.05).</p><p><b>Conclusion</b>NGF induces myofibroblast transformation but does not influence proliferation, cell cycle, or migration of CFs in vitro.</p>

Curcumin reduces cardiac fibrosis by inhibiting myofibroblast differentiation and decreasing transforming growth factor β1 and matrix metalloproteinase 9 / tissue inhibitor of metalloproteinase 1 / 中国结合医学杂志

<p><b>OBJECTIVE</b>To study the effect of curcumin on fibroblasts in rats with cardiac fibrosis.</p><p><b>METHODS</b>The rats were randomly divided into 4 groups (n=12 in each group): the normal control, isoproterenol (ISO), ISO combined with low-dose curcumin (ISO+Cur-L), and ISO combined with high-dose curcumin (ISO+Cur-H) groups. ISO+Cur-L and ISO+Cur-H groups were treated with curcumin (150 or 300 mg•kg•day) for 28 days. The primary culture of rat cardiac fibroblast was processed by trypsin digestion method in vitro. The 3rd to 5th generation were used for experiment. Western blot method was used to test the expression of collagen type I/III, α-smooth muscle actin (α-SMA), transforming growth factor (TGF)-β1, matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was applied to test the proliferation of fibroblast.</p><p><b>RESULT</b>Curcumin significantly decreased interstitial and perivascular myocardial collagen deposition and cardiac weight index with reducing protein expression of collagen type I/III in hearts (P<0.05). In addition, curcumin directly inhibited angiotensin (Ang) II-induced fibroblast proliferation and collagen type I/III expression in cardiac fibroblasts (P<0.05). Curcumin also inhibited fibrosis by inhibiting myofibroblast differentiation, decreased TGF-β1, MMP-9 and TIMP-1 expression (P<0.05) but had no effects on Smad3 in Ang II incubated cardiac fibroblasts.</p><p><b>CONCLUSIONS</b>Curcumin reduces cardiac fibrosis in rats and Ang II-induced fibroblast proliferation by inhibiting myofibroblast differentiation, decreasing collagen synthesis and accelerating collagen degradation through reduction of TGF-β1, MMPs/TIMPs. The present findings also provided novel insights into the role of curcumin as an antifibrotic agent for the treatment of cardiac fibrosis.</p>

HPLC characteristic chromatographic profile of Sarcandra glabra / 中国中药杂志

<p><b>OBJECTIVE</b>To develop the characteristic chromatographic profile of Sarcandra glabra by HPLC for its quality control.</p><p><b>METHOD</b>The HPLC analysis was performed on an Agilent Zorbax Eclipse XDB-C18 column (4. 6 mm x 250 mm, 5 microm) with column temperature at 40 degree C. The mobile phase was consisted of water containing 0. 5% formic acid and acetonitrile to methanol (1:9) in gradient mode, and the detection wavelength was set at 344 nm.</p><p><b>RESULT</b>A common mode of the HPLC characteristic chromatographic profile has been establised. There were 20 common peaks , seven of which were identified, and 46 samples from different habitats were classified into five groups based on principal component cluster analysis.</p><p><b>CONCLUSION</b>The method was time-saving and can represent the chemical information and provide a scientific basis for quality control of S. glabra.</p>

Protective function of melatonin to acute lung injury and its mechanisms in rats caused by oleic acid / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To observe the expression of P-selectin (Ps), intercellular adhesion molecule-1 (ICAM-1) and nuclear factor-kappa B (NF-kappaB) in lung tissues of acute lung injury (ALI) rat model induced by oleic acid (OA) and to explore the protective effects of melatonin (MT) in lung tissues in rats.</p><p><b>METHODS</b>All rats were randomly divided into four groups: control group, OA group, MT + OA group and SB203580 + OA group. Rat model of ALI was established by intravenous injection of oleic acid (OA). Lung coefficient was measured, lung tissues were imbedded by paraffin to observe morphological changes and the expression of Ps, ICAM-1 and NF-kappaB in lung tissues by means of immunohistochemistry staining.</p><p><b>RESULTS</b>Compared with control group, the lung coefficient increased significantly in OA group (P < 0.05). Alveolar septum thickened significantly in OA group, there had many infiltrated inflammatory cells and collapsed alveoli of lung; positive expression of Ps, ICAM-1 and NF-kappaB were very obvious (P < 0.05); the administration of MT and SB203580 mitigated above changes significantly (P < 0.05).</p><p><b>CONCLUSION</b>MT possesses obviously protective effect on lung tissues during ALI, its protective mechanism might be related to the inhibition of the expression of Ps, ICAM-1 and NF-kappaB.</p>

Protective effects of melatonin in acute lung injury rats caused by LPS / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To observe the expression of p-p38 mitogen-activated protein kinase in lung tissues of acute lung injury rat model induced by lipopolysaccharide (LPS) and to explore the protective effects of melatonin (MT) in lung tissues in rats.</p><p><b>METHODS</b>Seventy-two rats was randomly assigned to three groups, control group, LPS group and LPS + MT group. Rat model of ALI was established by instilling LPS intratracheally. We used immunohistochemical SP and Western blot method to detect the expression of p-p38 mitogen-activated protein kinase in lung tissues and used light microscope to observe morphological changes.</p><p><b>RESULTS</b>There were rare p-p38 mitogen-activated protein kinase positive cells scattered in alveolar and airway epithelial cells in control group (P < 0.01). The positive p-p38 mitogen-activated protein kinase cells in LPS group increased obviously than those in control group (P < 0.01), and were mainly distributed in infiltrative inflammatory cells, airway epithelial cells, alveolar epithelial cells and pleurames epithelial cells. In MT group, the p-p38 mitogen-activated protein kinase positive cells in airway and lung tissues were much less than those in the LPS group (P < 0.05). The Western blot results were consistent with those of immunohistochemical method.</p><p><b>CONCLUSION</b>The expression of p-p38 mitogen-activated protein kinase increases in alveolar and airway epithelial cells in acute lung injury rat models induced by LPS. The activation of p-p38 mitogen-activated protein kinase is found in most lung tissues, suggesting that p-p38 mitogen-activated protein kinase participates in the signal transduction in inflammatory and noninflammatory cells. MT is an effective antioxidant, which relieves the inflammation in acute lung injury rats, possibly through the inhibition of the pathway of p38 MAPK over activation.</p>

Role of polymorphonuclear neutrophil in exogenous hydrogen sulfide attenuating endotoxin-induced acute lung injury / 生理学报

The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NaHS group, LPS group and LPS + NaHS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected. The results showed that: (1) In in vivo study, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS + NaHS group (P<0.05, P<0.01); (2) In in vitro study, the apoptotic rates of PMN in LPS group and NaHS group were significantly higher than that in control group (P<0.01), while compared with LPS group, LPS + NaHS group showed significantly higher apoptotic rate (P<0.01). These results suggest that NaHS attenuates LPS-induced microvascular permeability and alleviates ALI. PMN apoptosis induced by NaHS is possibly one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.

Ameliorative effects of exogenous sulfur dioxide on lipopolysaccharide-induced acute lung injury in rats / 生理学报

To investigate the influence of sulfur dioxide (SO₂) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we examined the influence of exogenous SO₂ on pulmonary tissue inflammatory response. A rat model of ALI induced by intravenous (IV) injection of LPS was developed. Male Sprague-Dawley (SD) rats were divided into four groups randomly: control group, LPS group, LPS plus SO₂ group (IV injection of 0.5 mL Na₂SO₃/NaHSO₃ 10 min before LPS administration) and SO₂ group (only given Na₂SO₃/NaHSO₃). Animals were sacrificed 6 h after agent administration. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of lung tissues were observed. The number of polymorphonuclear neutrophil (PMN) in the bronchoalveolar lavage fluid (BALF), intercellular adhesion factor-1 (ICAM-1) expression in the lung tissue and IL-1, IL-6 and IL-10 levels in the serum were tested. The results showed that, compared to control rats, the LPS-treated rats had severe injuries of lung tissues and an increased LW/BW, increased index of quantitative assessment (IQA) score, increased PMN number in the BALF, increased ICAM-1 expression in the lung tissue and increased IL-1, IL-6 and IL-10 levels in the serum 6 h after LPS injection. Administration of the SO₂ donor, Na₂SO/₃NaHSO₃, into LPS-treated rats reduced the LW/BW, PMN number and ICAM-1 expression, and alleviated the degree of ALI (measured by the IQA score). In addition, Na₂SO₃/NaHSO₃ decreased IL-1 and IL-6 levels, but increased IL-10 level in the serum. There were no significant differences in the above indexes between SO₂-treated rats and control rats. These results suggest that exogenous SO₂ could inhibit the pulmonary tissue inflammatory response in rats with LPS-induced ALI.

Effects of melatonin on anti-oxidative function of lung injury induced by lipopolysaccharide in rats and ICAM-1 expression / 中国应用生理学杂志

<p><b>AIM</b>To investigate the protective effect of melatonin (MT) on lung tissues during acute lung injury (ALI) in rats and its possible mechanism.</p><p><b>METHODS</b>All rats were randomly divided into four groups: control group, lipopolysaccharide (LPS) group, dexamethasone (DEX) and MT treatment group. Myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity and malonaldehyde (MDA) content of lung tissues were detected at 3, 6 and 12 h after intratracheal instillation in each group. In addition, the expression of intercellular adhesion molecule-1 (ICAM-1) were observed through immunohistochemistry staining in lung tissues.</p><p><b>RESULTS</b>Compared with control group, SOD activity decreased significantly in LPS group (P < 0.01), but MPO activity,MDA content and the expression of ICAM-1 increased obviously (P < 0.01). The administration of MT and DEX mitigated above changes significantly (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>MT possessed protective effect on lung tissues during ALI through scavenging free radicals and inhibiting the expression of ICAM-1 probably.</p>

The protective function of puerarin to the injury of the lung and its mechanisms during diabetes / 中国应用生理学杂志

<p><b>AIM</b>To evaluate the roles of puerarin in alleviating the STZ-induced lung injury.</p><p><b>METHODS</b>DM model was established by streptozotocin (STZ) intraperitoneal injection to study the injury mechanisms of the lung. SD rats were divided randomly into control group (C group), diabetes group (DM group), diabetes + puerarin group (DM + Pur group). The blood glucose and weight were observed and recorded before and the 20 th, 40 th, 60 thd after administration of saline, STS, STZ+ Pur. Contents of NO and malondialdehyde (MDA) and activity of superoxide dismutase (SOD) were measured in lung tissues. Light microscope (LM), transmission electron microscope (TEM) and immunohistochemical analysis were also used.</p><p><b>RESULTS</b>(1) Compared with control group, the contents of NO and MDA were increased significantly (P < 0.01), while the activity of SOD reduced (P < 0.05). Compared with DM group, treatment with puerarin inhibited the increase of NO level (P < 0.01), and MDA content began to decline from 40 days after the model was established (P < 0.01), and inhibited the decrease of SOD activity induced by DM (P < 0.01). (2) LM and TEM results showed that alveolar and capillary basement membrane became thick, the number of tiny villus decreased markedly, the quantity of osmiophilic multilamellar body reduced remarkably, hyperplasia was shown in collgen fibre. Puerarin could alleviate above injuries induced by DM. (3) Immunohistochemical staining results showed that mild brown positive stain of NT could be seen in protoplasm of lung tissues. STZ administration induced the expression of NT in the protoplasm of cells, and led to stronger positive signals of NT than that of control group. Treatment with puerarin weakened the positive stain of NT.</p><p><b>CONCLUSION</b>(1) DM induced by STZ leads to a significant and sustained increase in blood glucose and obvious lung injury, which may be associated with the overproduction of free radicals. (2) The pathway of NO/ONOO- is one of the injury mechanisms of the lung tissues cells. (3) Puerarin suppresses the expression of NT and elevates the activity of SOD. Thereby, resulting in the reduces of the production of free radicals, which may be one of the mechanisms of its anti-oxidative-injuries.</p>

Protective role of endogenous carbon monoxide to lung and kidney tissues during septic shock / 中国应用生理学杂志

<p><b>AIM</b>To study the protective role of endogenous carbon monoxide to lung and kidney tissues during septic shock and its mechanism.</p><p><b>METHODS</b>A rat model of CLP was built by using the method of CLP. The malondialdehyde (MDA) content and the activity of superoxide dematase (SOD) in blood, lung and kidney were detected by immunohistochemical technique and light microscope.</p><p><b>RESULTS</b>Pathological changes of lung and kidney in CLP + Hemin group were lighter than CLP group, inflammatory reaction and lipid peroxidation were also lighter.</p><p><b>CONCLUSION</b>Endogenous CO can protect lung and kidney from the oxidative injury. It can suppress in flammation and the oxidative injury caused by activated inflammatory cells, it is probably an important mechanism of its protective effects.</p>