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In order to promote the innovative application of Sanjiao theory and Yingwei theory， this paper tries to apply the ''Sanjiao-Yingwei'' Qi transformation theory to the treatment of tumor diseases， integrating it with T cell exhaustion mechanism to elaborate on its scientific connotation and using network pharmacology and bioinformatics to elucidate the correlation between the anti-tumor mechanism of ''Sanjiao-Yingwei'' Qi transformation and T cell exhaustion. The ''Sanjiao-Yingwei'' Qi transformation function is closely related to the immunometabolic ability of the human body， and the ''Sanjiao-Yingwei'' Qi transformation system constitutes the immunometabolic exchange system within and outside the cellular environment. Cancer toxicity is generated by the fuzzy Sanjiao Qi， and the long-term fuzzy Sanjiao Qi is the primary factor leading to T cell exhaustion， which is related to the long-term activation of T cell receptors by the high tumor antigen load in the tumor microenvironment. Qi transformation malfunction of the Sanjiao produces phlegm and collects stasis， which contributes to T cell exhaustion and is correlated with nutrient deprivation， lipid accumulation， and high lactate levels in the immunosuppressed tumor microenvironment， as well as with the release of transforming growth factor-β and upregulated expression of programmed death receptor-1 by tumor-associated fibroblasts and platelets in the tumor microenvironment. Ying and Wei damage due to Sanjiao Qi transformation malfunction is similar to the abnormal manifestations such as progressive loss of exhausted T cell effector function and disturbance of cellular energy metabolism. Guizhi decoction， Shengming decoction， and Wendan decoction can correct T cell exhaustion and exert anti-tumor effects through multi-target and multi-pathways by regulating ''Sanjiao-Yingwei'' Qi transformation， and hypoxia inducible factor-1α （HIF-1α） may be one of the main pathways to correct T cell exhaustion. It was found that HIF-1α may be one of the important prognostic indicators in common tumors by bioinformatics. The use of the ''Sanjiao-Yingwei'' Qi transformation method may play an important part in improving the prognosis of tumor patients in clinical practice.
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Radiation-induced lung injury （RILI）， one of the common complications caused by radiotherapy， encompasses two phases： an early phase known as radiation pneumonitis （RP） and a late phase called radiation fibrosis （RF）， threatening the life and life quality of patients， with poor prognosis. Accumulating evidence has shown that the occurrence of RILI is related to a variety of cytokines and signaling pathways. This paper summarized the research on the effects of Chinese medicine on RILI from the perspective of cytokines and signaling pathways. Cytokines include transforming growth factor-β1 （TGF-β1）， interleukins （ILs）， tumor necrosis factor-α （TNF-α）， platelet-derived growth factor （PDGF）， vascular endothelial growth factor （VEGF）， and high mobility group box-1 （HMGB1）. Related signaling pathways are phosphatidylinositol-3-kinase/protein kinase B（PI3K/Akt） signaling pathway， mitogen-activated protein kinase （MAPK） signaling pathway， Wnt/β-catenin signaling pathway， Notch1/Jagged1 signaling pathway， and nuclear factor-E2-related factor2/antioxidant response element （Nrf2/ARE） signaling pathway. Cytokines may interfere with RILI progression by initiating various downstream signaling pathways， such as TGF-β1/Smads signaling pathway， TGF-β1/VEGF signaling pathway， TNF-α/nuclear factor-κB （NF-κB） signaling pathway， and HMGB1/Toll-like receptor 4 （TLR4） signaling pathway. In recent years， many scholars have attempted to delay RILI progression by down-regulating the expression of cytokines， antagonizing the effect of cytokines or regulating signaling pathways. It has been verified that many Chinese medicines， Chinese medicine monomers， and compound Chinese medicine prescriptions can inhibit the release of some cytokines or regulate some signaling pathways to reduce the incidence/severity of RILI， with satisfactory therapeutic effects， which have attracted the interest of scholars.
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OBJECTIVE To investigate the effect of microRNA-129(miR-129)expression on malignant phenotypes of esophageal squamous cell cancer(ESCC) cells and its possible molecular mechanisms. METHODS The constructed miR-129-overexpressed vector (pGCMV/EGFP/miR-129) and negative control vector (pGCMV/EGFP/miR-NC) were stably transfected into ESCC cell lines (Eca109 and EC9706),respectively. Quantitative real-time PCR(qRT-PCR)was performed to detect the expression of miR-129. MTT and flow cytometry(FCM)assays were performed to analyze the effects of miR-129 on proliferation, cell cycle and apoptosis of ESCC cells. Furthermore,a luciferase reporter vector with the putative B-cell lymphoma-2(Bcl-2)3′-untranslated region(pLUC/Bcl-2-3′-UTR-wt and pLUC/Bcl-2-3′-UTR-mut)was constructed to explore whether Bcl-2 was a direct target gene of miR-129 by detecting luciferase activity. Next,Western blotting was performed to detect the expression of Bcl-2, cleaved caspase 3 and total caspase 3 proteins. RESULTS Overexpression of miR-129 significantly inhibited proliferation(P<0.01),induced cell arrest in G0/G1 phase(P<0.05)and enhanced apoptosis (P<0.05)in ESCC cells. Luciferase reporter assay indicated that Bcl-2 was identified as a direct target gene of miR-129. Results of Western blotting showed that overexpression of miR-129 significantly reduced the expression of Bcl-2 protein and increased the expression of cleaved caspase 3 protein,but induced no changes in total caspase 3 protein in ESCC cells. CONCLUSION miR-129 functions as a tumor suppressor in ESCC cells by targeting Bcl-2 gene. Therefore,miR-129 will be a potential molecular target for the treatment of human ESCC.
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Hedyotis diffusa is an antioxidant, antibacterial Chinese herbal medicine which has anti-tumor, antioxidant, antibacterial, enhance the effect of nonspecific immunity and protection of the nervous system. Clinical application shows thatHedyotis diffusa has good efficacy on treatment of malignant tumors and inflammatory diseases. Referred to some papers published at home and abroad, this paper summarized from the aspects of active ingredient and antitumor effect. Results showes that its anti-tumor effect exactly, anti-tumor mechanism may be associated with a variety of molecular mechanisms, which remains to be further in-depth study.
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Leech has a broken blood stasis effect and has been used to eliminate a variety of stasis diseases. With the development of modern pharmacology study, in recent years, leeches are widely used in clinical cancer patients, and its anti-tumor effects have been confirmed by numerous clinical and experimental studies. Based on the latest domestic and foreign literature analysis and summary, this article discussed the antitumor mechanisms of leech from the following aspects:inhibition of tumor growth and proliferation, induction of tumor cell apoptosis, inhibition of tumor angiogenesis, anti-platelet aggregation and anti-clotting effect, improvement of immunity, and anti-tumor multi-drug resistance. It also pointed out deficiencies and controversy in current studies, with a purpose to provide ideas for further researches and clinical applications.
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This paper was aimed to discuss the mechanism of aristolchic acid toxicity, pathogenesis and possible causes of aristolchic acid nephropathy. Recent published studies both at home and abroad were summarized on the impact of aristolchic acid on the incidence and progression of aristolchic acid nephropathy. The results showed that traditional Chinese medicine (TCM) containing aristolchic acid was closely associated with the incidence of aristolchic acid nephropathy. It was concluded that the paper provided some suggestions on preventing aristolchic acid nephropathy.
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Objective:This study aimed to explore the effects of trichosanthin on the proliferative inhibition and apoptosis induc-tion in human lung carcinoma A549 cells. Methods:A549 cells were treated with various concentrations of TCS. The inhibitory effects in proliferation were detected by the MTT method. The microfilament changes were observed by transmission electron microscopy. Apoptosis rate and cell cycle were determined by flow cytometry. Results:A549 cells treated with TCS presented apoptotic changes and decreased cell activity. When the concentration increased and time was prolonged, the inhibition rate increased correspondingly. Conclusion:Pharmacological doses of TCS inhibited the proliferation and differentiation in lung carcinoma A549 cells and affected the function in A549 cells by changes in the cytoskeleton.
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Aim To investigate the proliferative effect and the apoptosis of human hepatoma SMMC-7721 cells induced by gallic acid ( GA ) , and its underlying mechanism. Methods SMMC-7721 cells were cul-tured in vitro. MTT assay was used to observe the pro-liferation of SMMC-7721 cells induced on GA 24 , 48 , 72 h. The morphological and ultra structural changes of the SMMC-7721 cells were observed by inverted micro-scope and transmission electron microscope respective-ly. Annexin V-FITC/PI staining was used to quantify the percentages of apoptosis in the total cell popula-tion. The expression of p53 mRNA was investigated by RT-PCR. Western blot was used to determine the pro-tein expression of p53. Results GA(6. 25~50 μmol ·L-1 ) markedly inhibited the activity of proliferation and induced apoptosis of SMMC-7721 cells after 48 h in a dose-dependent manner. GA significantly induced cell nuclear condensation and fragmentation. RT-PCR and Western blot results showed that GA could improve the expression of p53 mRNA and protein. Conclusion GA can inhibit the proliferation of human hepatoma SMMC-7721 cells and induce cells apoptosis. The mechanism may be associated with improving tumor suppressor gene p53 expression.
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Objective: To investigate the effects of Liangxue Tongyu Formula (LXTYF), a compound traditional Chinese herbal medicine, on brain edema in rats with intracerebral hemorrhage and to explore the mechanism. Methods: Intracerebral hemorrhage was induced by using the intrastriatal autologous blood injection. Rats were randomized into sham-operated (SO) group, intracerebral hemorrhage (ICH) group and LXTYF group. Rats in the LXTYF group were intragastrically administered with LXTYF every day while the other two groups were given normal saline. Brain water content was determined at 24, 48, 72, and 120 h after intracerebral hemorrhage. Matrix metalloproteinase-9 (MMP-9) level, and MMP-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA expressions in perihematoma area were detected by gelatin zymography and fluorescence quantitative real-time polymerase chain reaction at the four time points, respectively. Results: Water content in the ICH group was highly elevated after intracerebral hemorrhage, and reached to the peak at 72 h. Compared with the ICH group, the LXTYF group had lower water contents at 48, 72 and 120 h after intracerebral hemorrhage (P<0.01). The difference in water content between the LXTYF and SO groups was significant only at 72 h (P<0.01). Although the pro-MMP-9 level and MMP-9 activity in the LXTYF and ICH groups were enhanced, they were still lower in the LXTYF group than in the ICH group (P<0.01 for 24, 48, 72 and 120 h, respectively). And there was no significant difference in them between the LXTYF group and the SO group at 120 h. Meanwhile, MMP-9 mRNA expressions were increased in the ICH and LXTYF groups, but the levels in the LXTYF group were significantly lower (P<0.01 for 48, 72 and 120 h, respectively) than those in the ICH group. Also, TIMP-1 mRNA expressions at 24, 48, 72 and 120 h after intracerebral hemorrhage were up-regulated in the LXTYF group, and there were significant differences in TIMP-1 expressions between the LXTYF group and ICH group after intracerebral hemorrhage (P<0.01). Conclusion: Liangxue Tongyu Formula ameliorates brain edema in rats after intracerebral hemorrhage by inhibiting MMP-9 expression and activity and up-regulating TIMP-1.
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‘Stasis-heat’is a pathological factor that arises from exogenous and endogenous injuries in the development and progression of diseases.It can also be the pathogenesis at a certain stage of disease.It manifests clinically as the syndrome of‘Stasis-heat Interactivity.’Through long-term clinical practice‘Stasis-heat’has been found to spread in a variety of diseases’processes and has general clinical significance.Using‘Stasis-heat’theory in prescribing an herbal formula can significantly improve clinical efficacy,displaying the advantages of using traditional Chinese medicine to prevent and treat acute and severe diseases.According to more than 30 years of research and clinical practice,based on ongoing discussion and revision by experts,we have developed the‘Guide to TCM Syndrome Differentiation and Treatment of Stasis-heat Interactivity Syndrome,’a work that is an essential reference for both Chinese medicine and integrated Chinese and Western medicine clinicians.This article lays the groundwork in the hope that other experts will provide further input that will improve the guidelines laid out in this piece of work.
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To elucidate the academic thought of Professor ZHOU Zhong-ying about cancerous toxin. Professor Zhou holds that the cancerous toxin,a toxic pathogen occurring during the occurrence and development of malignant tumor,is the key for occurrence of malignant tumor. The compound pathogeneses of malignant tumor are the coexistence,reciprocal causation,combination and transformation between the cancerous toxin and the pathological factors of phlegm,blood stasis and dampness. Based on the theory of cancerous toxin,the therapeutic rules of malignant tumor should be removing carcinoma and eliminating toxin,supporting vital qi to eliminate pathogens,and combined the resolving phlegm,removing blood stasis,eliminating dampness or clearing away heat according to the different pathological factor accompanying,such as phlegm,blood stasis or dampness,etc.
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The chief cause of cancerous pain include six climate exopathogens,internal damage by excess of seven emotions,improper diet and deficiency of vital qi.Accumulation of cancerous toxin,intermingled phlegm and blood stasis and obstruction of meridians are the basic pathogenesis of cancerous pain,among which the accumulation of cancerous toxin is the key point of the pathogenesis,and phlegm and blood stasis are main pathological factors,the both are cause and effect for each other.The deficiency of vital qi is the internal factor of the disease.The location of disease concerns the relative viscera and meridians.The nature of disease is deficiency in the "root" and excess in the "branch" and excess in the "branch" is the main aspect.The therapeutic rules of the disease are removing toxic substance and removing stasis,resolving phlegm to dredge collaterals.And removing cancerous toxin is the crux of the therapy,and resolving phlegm to removing stasis should be applied from the beginning to the end.