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Osteoporosis is characterized by reduced bone mass and impaired micro-architectural structure, leading to an increased susceptibility to fractures. It is a complex, multifactorial disorder resulting from genetic factors, environmental factors and gene-environment interactions. Currently there are three opinions on the main pathogenesis of primary osteoporosis in traditional Chinese medicine: kidney deficiency, spleen deficiency, and spleen-kidney deficiency, in which disagreement remains. In this paper, the authors combine the modern etiology of osteoporosis to explain scientific connotation of the three opinions, aiming to comprehend the pathogenesis of primary osteoporosis and strengthen the communication between traditional Chinese medicine and Western medicine, and trying to evaluate the clinical curative effect on osteoporosis.
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In order to reveal the treatment mechanism of Chinese medicine with the effect of activating blood and resolving putridity, we selected acetyl-11-keto-beta-boswellic acid (AKBA) and arsenic trioxide (ATO), the main monomeric components of frankincense and arsenolite which are two most commonly used Chinese medicine with effect of activating blood and resolving putridity. We combined AKBA and ATO as a compound, and explored its regulatory role in productions and activities of matrix metalloproteinase (MMP)-1, MMP-2 and MMP-9 in human skin fibroblasts (HSFbs) and human acute monocytic leukemia cell line THP-1 in inflammatory state.
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Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases, which as a group can degrade essentially all extracellular matrix components. The proteolytic property of the MMPs is important during wound healing to remove debris and facilitate cell migration. Targeting towards the decreased MMPs activities is a new treatment strategy for healing chronic wounds. Salvia miltiorrhiza is a popular Chinese herb that could promote chronic ulcers healing for topical use. Salvianolic acid B (Sal B) is the most abundant bioactive component in Salvia miltiorrhiza. The research was designed to explore the inhibitory effects of Sal B on MMP-1, MMP-2 and MMP-9 activities.
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AIM: To evaluate the effects of acetyl-11-keto-beta-boswellic acid (AKBA, a main active component from frankincense, one of the traditional Chinese herb for healing wounds) on the activities of matrix metalloproteinase(MMP)-1, MMP-2 and MMP-9.METHODS: Pure human interstitial collagenase (MMP-1) or gelatinase A (MMP-2) was activated by p-aminophenylmercuric acetate (APMA), and was incubated with AKBA for 1 h. The activities of the enzymes were observed by quenched fluorescent substrate. The lysates of rat polymorphonuclear neutrophils [PMNs, rich in gelatinase B (MMP-9)] was incubated with AKBA for 1 h, and activity of MMP-9 was tested by gelatin zymography. Three cell models: activated human dermal fibroblasts by TNF-α, activated THP-1 cells by PMA and fibroblasts-THP-1 co-culture system were established. AKBA was cultured with these cell models for 24 h. The levels of MMP-1, MMP-2 and MMP-9 in the cell culture supernatants were tested by ELISA and activities of MMP-2 and MMP-9 were tested by gelatin zymography assays.RESULTS: AKBA dose-dependently inhibited the activities of human MMP-1 and MMP-2 at the range of 0.1-0.8 mmol/L, with 50% inhibitory concentration (IC50) of 0.18 mmol /L and 0.27 mmol/L, respectively. In the range of 0.05-0.85 mmol/L, AKBA inhibited the MMP-9 activity (P<0.01). Although AKBA promoted fibroblasts to secrete MMP-2, the production of MMP-9 by THP-1 was inhibited. In the cell co-culture system, the inhibitory effects on MMP-1, MMP-2 and MMP-9 productions were also observed.CONCLUSION: AKBA, as a bioactive component of frankincense, has an inhibitory effect on MMPs production and activities, indicating the possible mechanism for healing chronic wounds by frankincense.
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OBJECTIVE: To observe the effects of Tribulus terrestris L. saponion (TTLS) on apoptosis in cortical neurons induced by hypoxia-reoxygenation in rats. METHODS: Primary culture of rat cortical neurons was performed in vitro. A model of apoptosis of cortical neurons was established by hypoxia and reoxygenation. Hypoxia for 3 h in neural cells was induced with mixture of 95% N(2) and 5% CO(2), and then reoxygenation in neural cells was induced with mixture of 95% O(2) and 5% CO(2) for 12 h. Different concentrations of TTLS were administered to traditional Chinese herbal medicine-treated group separately during hypoxia and reoxygenation. The apoptosis rate was analyzed quantitatively by flow cytometry with Annexin V-FITC and propidium iodide staining. Mitochondria membrane potential was observed by a confocal laser-scanning microscope with JC-1 fluorescence. Caspase-3/7 activity in cytoplasm was measured by fluorescent plate reader. Bax protein expression was observed by immunohistochemical technique. RESULTS: The percentage of apoptosis was significantly increased, mitochondria membrane potential was obviously decreased, fluorescence of caspase-3/7 activity was increased, and Bax protein was abundantly expressed followed by 3 h of hypoxia and 12 h of reoxygenation (P<0.01). TTLS could inhibit the depression of membrane potential induced by hypoxia and reoxygenation, decrease the activity of caspase-3/7, reduce the expression of Bax protein, and inhibit the apoptosis of the cortical neurons. CONCLUSION: Hypoxia and reoxygenation can induce apoptosis of rat cortical neurons. TTLS can decrease the apoptosis induced by hypoxia and reoxygenation. The mechanism might be related to stabilization of mitochondria membrane potential, inhibition of caspase activity and reduction of Bax protein expression.
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AIM: To study the effect of berberine(Ber) on invasion and migration of PG cells from a high metastatic human giant lung carcinoma cell line and to explore its mechanism. METHODS: Agarose drop method was used to detect PG migration; transwell cabin with FN in lower chamber was adopted to detect PG chemotaxis. PG adhesion to FN and martrigel was detected by MTT; PG invasive ability was determined by transwell cabin covered with martrigel. Expression of MMP2/TIMP2 protein and mRNA were detected by quantitative immunocytochemical method and RT - PCR respectively. RESULTS: After PG was treated by Ber( 10 mg/L) for 24 h: 1 ) migration distance of Ber- treated PG cells was markedly shorter than that of control cells (P ＜0. 01 ) and the number of passed membrane cells towards FN was much fewer than that of control cells ( P ＜ 0. 01 ); 2) PG adhesion to FN and martrigel was inhibited remarkably by Ber compared with control PG; 3) the migration of PG cells through the martrigel -coated transwell was significantly inhibited by the addition of Ber; 4) MMP2 expression was reduced significantly(P ＜0. 01 ), while the TIMP2 expression showed up - regulating tendency, but had no differences compared with control group (P ＞ 0. 05). The MMP2/TIMP2 ratio was decreased; 5 )the MMP2 mRNA/TIMP2 mRNA ratio was decreased by Ber. CONCLUSION: Inhibition of cell migration, adhesion to ECM and invasion into ECM of tumor cells and regulation of homeostasis between MMPs and TIMPs to maintain ECM integrity may be the basic mechanism of inhibitive effect of Ber on invasion and metastasis of tumors.
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Vulnerable plaques is the hot spot in the researching field of cardiovascular diseases. In this paper, literature about establishment of experimental vulnerable plaques model animals published recent years were briefly reviewed and introduced concretely the conception, significance of researching, histopathologic characteristics of various types model, model assessment and current status of research.
Subject(s)
Animals , Mice , Coronary Artery Disease , Pathology , Coronary Vessels , Pathology , Disease Models, Animal , Mice, Inbred C57BLABSTRACT
Pathology and pathophysiology are sciences studying the laws and mechanisms of the occurrence and development of diseases, linking up the preclinical and clinical medicine. Owing to the different perspectives and ways of thinking, the western medicine and the traditional Chinese medicine developed respectively their independent theoretical, diagnostic and therapeutic systems. Integrative medicine, combining the theories and treatments of both western medicine and traditional Chinese medicine, has become the developing trend of medicine along with the social development. For this reason, pathological and pathophysiological research in integrated traditional Chinese and western medicine is highly significant for revealing the internal relations between the clinical manifestation and the pathological changes, for expounding the causes, conditions, mechanisms and laws of the occurrence and development of diseases. In doing related research, we should combine the disease and the syndrome, combine the macro-level and the micro-level, combine the part and the whole. We should manage to systematize the clinical research, to establish animal models of the syndromes, and to integrate the animal models of syndromes with the clinical characteristics of diseases. We should apply the theories of traditional Chinese medicine to the pathological and pathophysiological research of modern medicine.
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To study the direct effect of E.Coli endotoxin on the production of nitric oxide by endothelial cells, the second passage of cultured human umbilical cells was stimulated by serial doses of endotoxin (1 g/L, 10 mg/L, 100 μg/L, 10 μg/L, 1 μg/L), and the content of nitric oxide in supematant of culture and the viability of endothelial cells 6 hours after the stimulation were obcerved. The result showed that endotoxin had a slightly inhibitory effect on both the production of nitric oxide and the viability of endothelial cells at low doses (1 μg/L, 10 μg/L, 100 μg/L), especially the dose of 100 μg/L ［(608.63±11.64) μmol/L, versus that of unstimulated grouop (629.46±13.36) μmol/L, P＜0.05］. While the high doses of endotoxin exerted a big increasing in production of nitric oxide and a big decrease in the viability of endothelial cells, especially the dose of 1 g/L (NO: 722.58 μmol/L±32.18 μmol/L, versus that of unstimulated group P＜0.01; viability: 73.63%±8.50%, versus that of unstimulated group, P＜0.01). These could be concluded that low doses of endotoxin mainly resulted in functional changes in endothelial cells, such as decrease in relaxing factor (nitrc oxide), while high doses endotoxin exerted lethal effects on endothelial cells accompanied with high production of nitric oxide, which might be related to the death of cells.
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AIM and METHODS: To investigate the effect of endotoxin on the celluar activity and secretion of endothelin-1 by radioimmunoassay and MTT methods in cultured human umbilical vein endothelial cells stimulated by E coli endotoxin (E coli O55:B5, Sigma) of various concentrations (1 g/L, 100 mg/L， 10 mg/L，1 mg/L，100 μg/L，10 μg/L, 1 μg/L) and at the same time interval (HUVEC stimulated by endotoxin for 6 hours) in vitro.RESULTS:Endotoxin showed a slightly inhibitory effect on the viability of endothelial cells at low doses (1 μg/L， 10 μg/L, 100 μg/L, 1 mg/L). The viabilities were 92.00%±1.45%， 91.81%±2.03%, 89.52%±1.49%, 88.35%±1.88%, respectively, versus control group, P＜0.01. The cells were impaired significantly at the higher dose of LPS (100 mg/L), the viability was 80.49%±8.76%, versus control group, P＜0.01. The cells were killed evidently at the concentration of LPS (1 g/L), the viability was 73%±8%, versus control group, P＜0.01. The secretion of ET-1 increased gradually with the concentration of endotoxin manifolding. The concentration of ET-1 reached its peak at the dose of 100 μg/L, and it was (324.384±17.023) ng/L, versus control group (251.636±17.023) ng/L, P＜0.01. Endotoxin was effective in stimulating the endothelial cells to secret ET-1 in a dose dependent manner. CONCLUSION: These findings suggested ET-1 may be one of the important factors in endotoxic shock, and the increase in plasma ET-1 level in endotoxemia may be associated with increase in ET-1 secretion.
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AIM: To explore the mechanism of Nao-re-qing oral liquid (NRQ) decreasing endotoxin (ET)-induced fever in rabbits. METHODS: (1) The ET-induced fever model was established in rabbits. Febrile response of rabbits was observed. (2) The arginine vasopressin (AVP) content in the ventral septal area (VSA),and cAMP content in hypothalarmus (HP) and CSF were determined by radioimmunoassay.RESULTS: (1) In ET group,the maximal increment in body temperature (?T) [(1.80?0.16) ℃],6 h thermal respone index (TRI_6)(11.31?0.20),the cAMP content in the HP [(1.35?0.21)nmol/g],the cAMP content in CSF [(66.69?1.82) nmol/L] and AVP content in the VSA [(30.80?9.59)ng/g ] were significantly higher than those in NRQ+ET group[?T(0.82?0.08) ℃,TRI_6(5.73?0.09),HP: cAMP(0.70?0.50)nmol/g,CSF: cAMP(56.86?1.34),AVP:(11.91?3.47)ng/g]( P
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AIM: To explore the antipyretic mechanism of Qing Kai-Ling (QKL) injection on endotoxin (ET)-induced fever in rabbits. METHODS: Rabbit models of endotoxin (ET)-induced fever were duplicated. The rectal temperature was measured by digital thermograph. The cAMP and IL-1? content in the hypothalamus (HP), the cAMP content in the cerebrospinal fluid (CSF), and the arginine vasopressin (AVP) content in the ventral septal area (VSA) were determined by radioimmunoassay. RESULTS: ① QKL had significant antipyretic effect on ET-induced fever( P
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AIM: To detect the effects of Xinmailing Solution and MK-801 on injury of neuronal cell induced by glutamate. METHODS: Cultured neuronal cell injuried by glutamate was prepared and the content of malondialdehyde and nitrite in cell supernatant was measured. Morphology changes were also observed with discrepancy microscope at the same time. RESULTS: Xinmailing Solution and MK-801 attenuated cell injury induced by glutamate,and inhibited increase in malondialdehyde and nitrite in cell supernatant. CONCLUSION: Xinmailing Solution had a protective effect on neuronal cell at cell level.
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AIM: The effects of Jiere Xingshen(JRXS) Injection on cAMP, IL-1 ? content in hypothalamus (HP) of endotoxin(ET)-induced feverish rabbits were studied. METHODS: The ET-induced fever model was established in rabbits and the cAMP content in hypothalamus (HP) and csf, IL-1 ? content in HP were determined by radioimmunoassay following intravenous infusion of JRXS. RESULTS: In ET group, the ?T [(0 40?0 11)℃], TRI 1(1 78?0 79), cAMP content in HP [(2 90?0 40) nmol/g], cAMP content in csf [(32 10?4 51) nmol/L)], IL-1 ? content in HP[(6 08?0 79) ng/g] were higher than that of NS and JRXS+ET group ( P
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AIM: To establish a model of primary cultured neuron injury induced by D-galactose for the research in Alzheimer's disease. METHODS: Primary rat neurons cultured for 6 days were exposed to 50 mmol D-galactose for 72 h. The neural growth and neurite density were observed with HE stain and microscope, the neural metabolism rate and apoptosis rate were examined with MTT, immuno-enzyme assay and flow cytometry, respectively, and the aldose reductase mRNA expression was also detected with RT-PCR. RESULTS: The neural growth and development in neurons treated with D-galactose was retarded, the neural metabolism rate decreased from 0.762?0 030( n= 33) to 0 543?0 064( n= 11)( P
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AIM: To study the effect of Aima recipe (AM), a traditional Chinese medicine, on the protein and mRNA expression of TNF? and ICAM-1 in the bronchus of rats with chronic bronchitis(CB). METHODS: 15 male Wistar rats were randomly divided into three groups: control group, chronic bronchitis (CB) group, CB plus AM group. The protein and mRNA expression of TNF? and ICAM-1 were assayed by immunohistochemistry and in situ hybridization methods. RESULTS: TNF?, ICAM-1 protein and mRNA were more strongly expressed in the area of bronchial epithelium in the CB group compared with control group ( P
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AIM: The aim of this work is to investigate the protective effects of Ginsenoside Rb 1(Rb 1) on apoptosis induced by hypoxia /hypoglycemia and reoxygenation in cultured rat hippocampal neurons. METHODS: Apoptosis were measured by flow cytometry; Morphological changes and neuronal necrosis were examined under microscope; The leakage of lactic dehydrogenase(LDH) and the product of nitric oxide(NO) were measured. RESULTS: hypoxia /hypoglycemia cultures for 5 h and reoxygenation induced neuronal apoptosis and necrosis,and significantly increased the leakage of LDH and the product of NO. The effects were enhanced with the extending time of reoxygenation. Rb 1 could significantly decrease the percentage of neuronal apoptosis and necrosis, and reduce the leakage of LDH and the product of NO. CONCLUSION: Rb 1 had an effect of anti-neuronal apoptosis. This effect might be related to the inhibition of the activity of NO synthase and NO production.
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AIM: To observe the changes in neuropeptide Y(NPY) and the effect of Fu-Sheng powder(FSP) on NPY in the rat brain in a steady cerebral ischemia and reperfusion(I/R) model. METHODS: The models of rat brain injury were established by repeated cerebral I/R in rats with hyperlipidemia. Radioimmunoassay was performed to determine the level of NPY, while NPY mRNA expression was observed by in situ hybridization. RESULTS: After 1 day of I/R, compared with control group, the content of NPY in the model animals were significantly increased by 51.86% ( P
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AIM: To observe the direct effect of lipopolysaccharide (LPS) on secretion of endothelin-1(ET-1) and nitric oxide by human umbilical vein endothelial cell and cell viability of the secretor. METHODS: The third passage of human umbilical vein endothelial cells were incubated with different concentrations of LPS(1 g/L, 100 mg/L, 10 mg/L, 1 mg/L, 100 ?g/L, 10 ?g/L, 1 ?g/L) for 6 hours, and the culture supernatants were collected. The concentrations of ET-1 were determined by radioimmunoassay, the concentrations of nitric oxide were determined using Greiss's method. The viabilities of cells were measured by MTT method. RESULTS: The concentration of ET-1 (pg/L) of normal control group was 251 64?10 90. The concentrations of ET-1(pg/L) of LPS treated groups were 220 85?19 14, 278 67?15 45, 306 40?11 60, 312 87?33 50, 324 38?17 02, 291 49?14 30, 282 11?13 38, respectively. (each group compared with normal control group, P
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AIM: To explore the influence of herbs (9602 prescription) on brain energy metabolism in cerebral ischemia reperfusion mice.METHODS: Ischemia reperfusion in cerebral injury model was duplicated in mice. Using nuclear magnetic resonance (NMR) and high performance liquid chromatography (HPLC), the brain metabolism were measured. The influence of 9602 prescription on cerebral energy metabolism in ischemia reperfusion mice model was dynamicly observed. RESULTS: Phase Ⅰ: The spectrum of NMR showed that after 10 min of ischemia, the PCr peak dropped significantly, while the Pi peak rose significantly in both the control and the “9602” group. There was no remarkable difference between the two groups. After reperfusion the PCr peak in the control group continued dropping slowly and remained at a low level (55.50?14.94) after 10 min of reperfusion, while after reperfusion the fallen PCr peak in the “9602” group started rising till 76.72?13.37 (P0.05). Phase Ⅱ: The HPLC showed that the cerebral energy charge values of the control group (0.1104?0.0343) were significantly lower than those of the “9602” group (0.2884?0.0552) and the sham-operation group (0.1846?0.0455) (P