ABSTRACT
Atherosclerosis(AS) is the key pathological basis of coronary heart disease(CHD), and lipid infiltration is a classical theory to explain the pathological mechanism of AS. The theory highlights that the occurrence and development of AS are closely related to abnormal lipid metabolism, with the essence of the pathological reaction caused by the invasion of lipids into arterial intima from plasma. Phlegm and blood stasis are physiologically homologous and subject to pathological co-existence. Phlegm-blood stasis correlation is the basic theory to explain the pathogenesis characteristics of CHD and has important guiding significance for revealing the mecha-nism of lipid infiltration of CHD. Phlegm is the pathological product of abnormal metabolism of Qi, blood, and body fluid, and a gene-ral summary of a series of abnormally expressed lipid substances. Among them, turbid phlegm invades the heart vessels, gradually accumulates, and condenses to achieve the qualitative change from "invisible pathogen" to "tangible pathogen", which corresponds to the mechanism of lipid migration and deposition in the intima of blood vessels, and is the starting factor of the disease. Blood stasis is the continuous development of phlegm, and it is a result of pathological states such as decreased blood fluidity, increased blood coagulation, and abnormal rheology. The fact that blood stasis caused by phlegm accords with the pathological process of "lipid abnormality-circulatory disturbance" and is the central link of the disease. Phlegm and blood stasis aggravate each other and lead to indissoluble cementation. The phlegm-blood stasis combination serves as common pathogen to trigger the disease, which is the inevitable outcome of the disease. Based on the phlegm-blood stasis correlation theory, the simultaneous treatment of phlegm and blood stasis is established. It is found that this therapy can simultaneously regulate blood lipid, reduce blood viscosity, and improve blood circulation, which can fundamentally cut off the biological material basis of the reciprocal transformation between phlegm and blood stasis, thus exerting a significant curative effect.
Subject(s)
Humans , Medicine, Chinese Traditional , Coronary Disease , Mucus , Atherosclerosis , LipidsABSTRACT
Objective • To explore the effect of inhibiting transforming growth factor β (TGF-β) signaling pathway on the stem cell-mediated liver regeneration in mice after partial hepatectomy (PH). Methods • Eighteen C57BL/6 male mice were selected to establish the model of hepatectomy. mRNA and protein levels of the signal molecules in TGF-β pathway, as well as stem cell markers α-fetoprotein (AFP) and leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5) in the liver tissues were detected before (PH0) and on the 1st (PH1), 3rd (PH3) and 7th (PH7) day after operation. Then, additional 32 mice were assigned into inhibitor group [PH+SB-431542, 10 mg/(kg•d)] and control group (PH+normal saline). The mice were sacrificed on the 1st (PH1) and 3rd (PH3) day after operation and liver remnants were obtained. Realtime-PCR, Western blotting, and immunofluorescence staining were used to detect the expressing variation of TGF-β signaling pathway, AFP and LGR5. Results • The mRNA and protein expression of TGF-β1, phosphorylated SMAD2 (p-SMAD2) protein, Afp mRNA, the number of AFP immune-positive cells and Lgr5 mRNA were upregulated significantly after PH, peaked at PH3 (P<0.05) and recovered to pre-operative level at PH7. Compared with control group, the above indices were all obviously inhibited in inhibitor group at PH3 (P<0.05). Conclusion • TGF-β signaling pathway may regulate the stem cell-mediated liver regeneration in mice after PH.
ABSTRACT
BACKGROUND: Difficulty in long-time survival and continuous proliferation is the main problem for transplanted fetal hepatic progenitor cells and co-transplantation with transforming growth factor beta 1 (TGF-β1)-induced hepatic stellate cells may be a promising way to solve this scientific obstacle. OBJECTIVE: To explore the therapeutic effects of co-transplantation of fetal hepatic progenitor cells and TGF-β1-induced hepatic stellate cells on acute liver injury in mice. METHODS: Over-expression vector pHBLV-CMVIE-TGF-β1 was infected to mouse hepatic stellate cells and transfection efficiency was detected by immunocytochemistory, western blot and qRT-PCR. Hepatic progenitor cells, mHPCs-E14.5, were cultured and identified by immunofluorescence in vitro.The mouse model of acute liver injury was established by intraperitoneal injection of CCl4in combination with 2/3 partial hepatectomy, followed by mHPCs-E14.5transplantation, co-transplantation of mHPCs-E14.5and mHSCs-pHBLV-CMVIE-TGF-β1 (experimental co-transplantation group) or co-transplantation of mHPCs-E14.5and mHSCs-pHBLV-CMVIE-GFP (control co-transplantation group) for cell transplantation assay. Confocal immunofluorescence staining against CK19, ALB, a-SMA was performed to analyze the engraftment and differentiation of transplanted cells in the splenic parenchyma 14 days post-transplantation; serum alanine transferase and aspartate transferase levels were monitored using an automatic biochemistry analyzer. RESULTS AND CONCLUSION: (1) A hepatic stellate cell line that over-expressing TGF-β1 was successfully established and expression levels of TGF-β1 and α-smooth muscle actin were efficiently up-regulated in the over-expression group (P < 0.01). (2) mHPCs-E14.5expressed massive AFP and low levels of ALB and CK19,confirming that this cell line was in complete conformity with fetal hepatic progenitor cells in vitro.(3)CK19 and ALB positive cells existed in the splenic parenchyma in mHPCs-E14.5transplantation group.Highly expressed ALB but less expressed α-SMA and CK19 were observed in the control co-transplantation group, while massive CK19 and a-SMA positive cells as well as less level of ALB positive cells existed in the experimental co-transplantation group. Serum alanine transferase and aspartate transferase levels were decreased remarkably after cell transplantation, and moreover, the decrease was more obvious in the experimental co-transplantation group (P < 0.05). Overall, transplanted fetal hepatic progenitor cells engraft and differentiate into hepatocytes and cholangiocytes in the splenic parechyma successfully in vivo.Importantly,hepatic stellate cells induced by TGF-β1 promote the differentiation of fetal hepatic progenitor cells into cholangiocytes and accelerate recovery from CCl4/partial hepatectomy induced acute liver injury.
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To make clear the concept of reinforcing and reducing manipulations of acupuncture, so as to better instruct the clinical practice and enhance the therapeutic effect. Inspired by the dispute on stimulus quantity in reinforcing and reducing manipulations of the modern physicians, and on the basis of Huangdi Neijing (Huangdi's Canon of Internal Classic), relations between stimulus quantity and different manipulations were explored through studies on reducing and reinforcing experiences of outstanding modern physicians as well as the related scientific re searches. Taking references of both ancient and modern experiences, it is held that stimulus quantity can not be taken as the only index to describe the reinforcing and reducing manipulations of acupuncture, there is no corresponding relation between them. However, it has a certain positive significance on instruction of clinical practice and standardization of modern scientific researches.
Subject(s)
Humans , Acupuncture Therapy , History , Methods , China , History, Ancient , Medicine in Literature , Medicine, Chinese Traditional , History , MethodsABSTRACT
The study was aimed to investigate the immunophenotypic and cytogenetic features of chronic lymphocytic leukemia (CLL) in order to provide an evidence for diagnosis and therapy. Immunophenotypic analysis was performed by using a panel of monoclonal antibodies and three-color immunofluorescence staining methods of flow cytometry in 51 patients with CLL, and the cytogenetic features were analyzed by R-banding technique. The results indicated that among 51 CLL cases, the positive rate of CD19 and CD23 was 96.1%, followed by CD15 (94.1%), CD20 (82.4%) and CD22 (78.4%). The positive rate of CD38 was 23.5%. Forty-six patients expressed both CD5 and CD19. Seven main clonal chromosomal abnormalities were detected by conventional cytogenetics (CC) in eighteen cases (35.3%), with three cases of +12, two cases of 13q(-), other chromosomal abnormalities included +14, 6q(-), t (11; 14), t (14; 18) and t (2; 7). Expression of the antigens had no relationship with chromosomal abnormalities. It is concluded that typical CLL express CD5, CD19 and CD23, and the positive rate detected by CC in CLL is low. Immunophenotyping in combination with cytogenetic technique plays an important role in the diagnosis and prognosis of CLL.