Review of Modern TCM Oncology Academic Thought / 肿瘤防治研究

With the establishment of modern traditional Chinese medicine (TCM) as an oncology discipline, it has made great development and progress in the prevention and treatment of tumors. As a result, a number of academic thoughts and viewpoints have emerged. In the tumor field of TCM, the current representative theories include the theory of strengthening the body and treating cancer, the theory of treating from the membrane, the theory of surviving with tumor, the pathogenesis theory of cancer virus, the theory of consolidating the root and clearing the source, and the theory of regulating qi and detoxing. In TCM oncology, a large number of results have been achieved in the research of the thoughts of famous TCM doctors. However, discussions on these thoughts together are relatively few. This article summarizes and studies the above innovative theories from the aspects of academic connotation and clinical application to provide new ideas for further guiding the clinical practice of TCM oncology.

Discussion on the Treatment of Malignant Tumors by the Method of Counteracting Toxin with Toxin / 中医杂志

Cancer toxin is the key pathogenesis of malignant tumors. The basic principle of cancer treatment is “dispelling pathogen and resolving toxins， reinforcing healthy qi and reinforcing the foundation”. As one of the “eight methods of anticancer and detoxification”， the counteracting toxin with toxin therapy is a commonly used clinical treatment of malignant tumors. This paper discussed the method of counteracting toxin with toxin and its application in the prevention and treatment of malignant tumors from the aspects of history tracing， academic connotation， application principles and clinical application. Toxic Chinese medicinals with anticancer function are required to eliminate cancer toxins based on the principles of excessive cancer toxicity and plentiful healthy qi， as well as in accordance with the various stages and classifications of tumors， thereby improving the theoretical connotation of the method of counteracting toxin with toxin， and promoting the popularization and application of the pathogenesis theory of cancer toxin in the prevention and treatment of malignant tumors.

Shenbai Jiedu Prescription Inhibits Proliferation of Colorectal Cancer Cells by Regulating PTEN/PI3K/Akt Signaling Pathway / 中国实验方剂学杂志

ObjectiveTo study the mechanism of Shenbai Jiedu prescription inhibiting the proliferation of HCT116 colorectal cancer （CRC） cells by regulating the phosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/ protein kinase B （Akt） signaling pathway. MethodShenbai Jiedu prescription was extracted by water extraction and alcohol precipitation to prepare freeze-dried powder. HCT116 cells were cultured in vitro， and treated with different concentrations of Shenbai Jiedu prescription （2， 4， 8， 16 g·L-1）. The inhibitory effect of Shenbai Jiedu prescription on the proliferation of HCT116 cells was tested by methyl thiazolyl tetrazolium （MTT）. Real-time quantitative PCR was used to detect the mRNA expression levels of PTEN， PI3K， Akt， glycogen synthase kinase-3β （GSK-3β）， c-Myc， survivin and Cyclin D1. Western blot was employed to measure the protein expression levels of PTEN， phosphorylated PTEN （p-PTEN）， PI3K， Akt， phosphorylated Akt （p-Akt）， GSK-3β， phosphorylated GSK-3β （p-GSK-3β）， c-Myc， survivin and Cyclin D1， β-catenin nuclear import was explored by immunofluorescence assay. ResultCompared with the control group， Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner （P<0.01）. Compared with the control group， the mRNA expression levels of PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， c-Myc， survivin and CyclinD1 were down-regulated after treatment with Shenbai Jiedu prescription （P<0.01）. The protein expression levels of PTEN， p-PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， p-Akt， GSK-3β， p-GSK-3β， c-Myc， survivin and CyclinD1 were down-regulated （P<0.05， P<0.01）. Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed β-catenin nuclear import in HCT116 cells. ConclusionShenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.

Efficacy and Mechanism of Shenbai Jiedu Prescription Against Proliferation of HCT116 Cells / 中国实验方剂学杂志

ObjectiveTo investigate the mechanism by which Shenbai Jiedu prescription （SBJDF） inhibits the proliferation of colorectal cancer （CRC） HCT116 cells. MethodAfter 48 h treatment of HCT116 cells with SBJDF （0， 0.25， 0.5， 1， 2， 4 g·L-1）， the viability of HCT116 cells were determined by methyl thiazolyl tetrazolium （MTT） colorimetry. Following the classification of cells into blank control group and SBJDF （1， 2， 4 g·L-1） groups， the effect of SBJDF on HCT116 cell morphology was observed under an inverted microscope. The effects of SBJDF on the proliferation of HCT116 cells and mitochondrial membrane potential （Δψm） were detected by colony formation assay and JC-1 probe， respectively. The flow cytometry was then performed for determining cell cycle distribution and apoptosis. The effects of SBJDF on cell cycle-， apoptosis-， and nuclear factor kappa-B （NF-κB） signaling pathway-related proteins were determined by Western blot. ResultSBJDF effectively inhibited the vitality of HCT116 cells and changed their morphology in a concentration-dependent manner. Compared with the blank control group， SBJDF at 1， 2， 4 g·L-1 significantly reduced cell colony formation （P<0.05， P<0.01），and SBJDF at 2 and 4 g·L-1 arrested the HCT116 cell cycle at G0/G1 phase （P<0.05， P<0.01）. Compared with the blank control group， SBJDF at 1， 2， 4 g·L-1 remarkably down-regulated the protein expression of CyclinD1 （P<0.05， P<0.01）. SBJDF at 2 and 4 g·L-1 lowered the CyclinA2 and cyclin-dependent kinase 4 （CDK4） （P<0.05， P<0.01）. SBJDF at 4 g·L-1 reduced the cyclin-dependent kinase 1 （CDK1） （P<0.01）. Compared with the blank control group， SBJDF at 2 and 4 g·L-1 induced HCT116 cell apoptosis， down-regulated the protein expression of anti-apoptosis-related proteins Bcl-2 and Bcl-xl as well as the NF-κB signaling pathway-related proteins IκB kinase α （IKKα），inhibitor α of NF-κB （IκBα），and phospho-NF-κB p65 （p-p65） （P<0.05， P<0.01）， and diminished the mitochondrial membrane potential of HCT116 cells. ConclusionSBJDF inhibits the proliferation of HCT116 cells， which may be related to its inhibition of the activation of NF-κB signaling pathway and the induction of cell cycle arrest and apoptosis.

Allosteric inhibition reveals SHP2-mediated tumor immunosuppression in colon cancer by single-cell transcriptomics

Colorectal cancer (CRC), a malignant tumor worldwide consists of microsatellite instability (MSI) and stable (MSS) phenotypes. Although SHP2 is a hopeful target for cancer therapy, its relationship with innate immunosuppression remains elusive. To address that, single-cell RNA sequencing was performed to explore the role of SHP2 in all cell types of tumor microenvironment (TME) from murine MC38 xenografts. Intratumoral cells were found to be functionally heterogeneous and responded significantly to SHP099, a SHP2 allosteric inhibitor. The malignant evolution of tumor cells was remarkably arrested by SHP099. Mechanistically, STING-TBK1-IRF3-mediated type I interferon signaling was highly activated by SHP099 in infiltrated myeloid cells. Notably, CRC patients with MSS phenotype exhibited greater macrophage infiltration and more potent SHP2 phosphorylation in CD68+ macrophages than MSI-high phenotypes, suggesting the potential role of macrophagic SHP2 in TME. Collectively, our data reveals a mechanism of innate immunosuppression mediated by SHP2, suggesting that SHP2 is a promising target for colon cancer immunotherapy.

Fatal familial insomnia presenting with posture instability and retropulsion: a case report and literature review / 中华神经科杂志

Objective:To explore the clinical and genetic features in a case of fatal familial insomnia (FFI).Methods:A case of 39 years old woman diagnosed as progressive supranuclear palsy based on the preliminary manifestation of imbalance and frequent falls was reported. The clinical features, imaging characteristics, electroencephalogram and polysomnography of the patient were analyzed, and the blood samples from the patient were collected for the sequencing of prion protein (PRNP) gene.Results:This patient is a middle-aged woman, whose clinical manifestations were posture instability and retropulsion, rapid progressive dementia and dysarthria, sleep-related dyspnea and laryngeal stridor, with autonomic symptoms of hypertension, sweating, tachycardia and irregular breathing. The results of PRNP gene sequencing revealed that the mutation of gene D178N/129M was detected.Conclusions:Laryngeal stridor plays an important role in the diagnosis of FFI. Posture instability and retropulsion are relatively rare in the FFI clinical symptom spectrum. Here, a case of FFI presenting with posture instability and retropulsion during the early stage with Met/Met at the polymorphic codon 129 is reported in China.

Clinical Experience of Professor CHENG Haibo for Tumor Metastasis by Cancerous Toxin Pathogenesis Theory / 浙江中医药大学学报

[Objective]To summarize professor CHENG Haibo's clinical experience in treating tumor metastasis with cancerous toxin pathogenesis theory. [Method] By following the teacher clinic and sorting out the related cases,the author summarizes professor CHENG Haibo's academic experience of treatment of tumor metastasis with cancerous toxin pathogenesis theory,and for proven cases. [Result] On the base of cancerous toxin pathogenesis theory and clinical practice,Professor CHENG Haibo puts forward that deficiency of vital qi and cancerous toxin inflowis the basic pathogenesis of tumor metastasis. Qi deficiency is the root cause of tumor metastasis and canceousr toxin inflow is the main pathogenesis of tumor metastasis. Canceousr toxin inflow has special channel,carrier and law,and supporting and invigorating Qi,anti-cancer and detoxificationis the main method of prevention and treatment of tumor metastasis. Professor CHENG Haibo treated a case of brain and liver metastasis in lung cancer with cancerous toxin pathogenesis theory before. And the curative effect was very remarkable. Brain and liver metastasis was significantly reduced.[Conclusion] Professor CHENG Haibo 's experience is effective and worthy of learning and promotion.

Influence ofQing-Chang Hua-Shi Recipe on IL-6Trans-signaling in Experimental Colitis in Mice / 世界科学技术-中医药现代化

This study was aimed to observe the influence ofQing-Chang Hua-Shi Recipe (QHR) on IL-6trans-signaling in experimental colitis mice, in order to initially explore the possible mechanisms of QHR for ulcerative colitis (UC). TNBS/ethanol was used in the establishment of colitis mice model. After intervention of medication, ELISA was used in the detection of soluble Interleukin-6 receptor (sIL-6R). Real-time PCR was used to detect the mRNA expression level of IL-6 and glycoprotein 130 (gp130). Western blot was used in the observation of protein expression of IL-6 and gp130 in the colonic mucosa. The results showed that the level of sIL-6R, the mRNA and protein expression of IL-6 and gp130 in the model group were significantly higher than that in the control group. QHR was able to reduce the sIL-6R level (P < 0.01), decreased the mRNA and protein expression of IL-6 and gp130 (P < 0.01) in the colon tissues among experimental colitis mice. It was concluded that QHR had good anti-inflammatory effects on experimental colitis mice. It might be associated with influencing IL-6trans-signaling.

Discussion on the TCM theory of cancerous pain / 中华中医药杂志

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.

Discussion on academic thought of Professor ZHOU Zhong-ying about cancerous toxin / 中华中医药杂志

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.

Effect of Aitongping on c-fos Gene Expression and Substance P Content in Spinal Dorsal Horn of Rats with Formalin-induced Pain / 广州中医药大学学报

Objective To observe the effect of Aitongping on c-fos gene expression and substance P(SP) content in spinal dorsal horn of rats with formalin-induced pain.Methods Fifty SD rats were randomized into 5 groups: blank control group,model group,tramadol group(0.06g/kg),high-and low-dose Aitongping groups(36 and 18g/kg respectively).Rats model of pain was induced by subcutaneous injection of formalin into the plantar surface of the left hind paw of rats.The fos gene expression and SP content were observed in superficial lamella of spinal dorsal horn of spinal section from the lumbar vertebrae L3 to L5 by immunohistochemical method.Results The number of neurons with fos gene expression positive and the optical density(D value) of reactants with SP expression positive were increased in the model group(P