| Type 2 diabetic mellitus(T2DM) is belonged in Traditional Chinese Medicine(TCM)XiaoKe-Disease. Insulin Resistanc(IR) is an important one of pathogenesis and it is thecharacteristic of T2DM. Systematic studies on the prevention and treatment for T2DM,IR byJieDuTongLuoTiaoGanSan(JDTLTGS) had been performed from the aspects of referencereviews, theory discussion and experimental study in this essay. It layed stress on that themain mechanism of T2DM is inflammatory Pathogenesis in liver, exploring the relationbetween TCM pathogenetic theory of liver-collaterals impaired by Toxin and theinflammatory Pathogenesis in liver of T2DM,IR. While "Method of Removing toxin,activating collateral and regulating liver"being scientific is illustrated from a different angle.The experimental study clarifies inflammatory Pathogenesis in liver of T2DM,IR from TCMinhibitting expressed pathway of inflammatory factor in liver, increasing expression of Insulinreceptor substrate-2(IRS-2) protein and mRNA consequently which is practical andinnovative.1 Reference review1.1 The skeleton research of TCM on T2DM,IRThis essay reviewed from the advances of such fields as followed: the source and nameof TCM for T2DM,IR, the etiology and pathogenesis for T2DM,IR, selection of treatmentbased on the differential syndrome diagnosis, the pathogenesis of TCM on T2DM,IR, whichis in ancient and modern times, moreover, included the evaluations and prospects on theproblems lying in the selection of treatment based on the differential syndrome diagnosis orscientific study.1.2 The latest study of pathogenesis of T2DM,IRThe results and progresses of study on glucose and lipid metabolism, inflammatorypathogenesis and the nuclear factor-κB (NF-κB),the monocyte chemoattractant protein-1(MCP-1), and IRS-2 were summarized involving the inflammatory pathogenesis of T2DM,IRat home and abroad in recent years. 2 Theory StudyBy discussing the pathogenesis theory, principle and method of treatment of XiaoKeDisease with Chinese medicine theories quoting from the Chinese classics works, we putforward the theory that the main mechanism of XiaoKe Disease is Liver-collaterals impairedby Toxin. By combining modern research result, we put forward the theory that the mainmechanism of T2DM is inflammatory Pathogenesis in liver, while we investigate therelationship between inflammatory Pathogenesis in liver of T2DM,IR and TCMpathogenetic theory of liver-collaterals impaired by Toxin..Theory gist of treating XiaoKeDisease is provided by us discussing the effective way of "method for removing toxin,activating collateral and regulating liver" intervening inflammatory pathogenesis in Liver ofT2DM,IR.3 Experimental study3.1 The influence about JDTLTGS in the experimental diabetic ratsHigh fat and glucose food and STZ-induced diabetic rats were divided randomLy intonormal control group, diabetic model group, positive control group (DM+metformin,DM+pioglitazone), experimental group (DM+JDTLTGS) in Chinese herb. The various markswere observed. The results showed JDTLTGS obviously improve the rats' general conditionand had a certain effect on reducing blood glucose, increasing insulin sensitivity index, whichhad a significant statistic sense in comparing with diabetic model group (P＜0.01).Besides itcould lighten weight, reduce liver index,AST,ALT, which had a significant statistic sense incomparing with diabetic model group (P＜0.01).It also serumed cholesterol (TC) andtriglyceride (TG), the level of free fattty acid in blood and liver tissue, which had a significantstatistic sense in comparing with diabetic model group (P＜0.01). The results indicated thatJDTLTGS was beneficial for regulating glucose and lipid metabolism, increasing insulinsensitivity, improving liver function.3.2 The influence about JDTLTGS on the changes of liver tissue pathology in experimentaldiabetic ratsThe changes of liver tissue pathology in experimental diabetic rats were observed byimmunohistochemical method. The steatosis changes and inflammation activity of all rat livers were scored in optical microscope. The results showed:DM model group's liver tissue showedfatty change, inflammatory cells infiltration, hepatocyte necrosis partly. The liver tissuechange in the experimental group that cured by metformin,pioglitazone and JDTLTGSobviously improved, which have remarkable difference from the DM model group (P＜0.01)byfatty change and inflammatory scores in liver. The results indicated JDTLTGS can obviouslyimproved liver tissue pathological change, obviously inhibited DM model group's liver fattychange,inflammatory cells infiltration and protected DM model group's liver.3.3 The study about effect of JDTLTGS on NF-κB and MCP-1 pathway in experimentaldiabetic ratsIt was done that assaying the protein expression of NF-κB,MCP-1 in the experimentaldiabetic rats'liver tissue of each group by immunohistochemical method. Besides the mRNAexpression of MCP-1 in the experimental diabetic rats'liver tissue of each group by RT-PCRmethod. The results showed:the protein expression of NF-κB,MCP-1 and the mRNAexpression of MCP-1 in DM model group's liver tissue obviously increased, which haveremarkable difference from the normal control group (P＜0.01); the protein expression ofNF-κB,MCP-1 and the mRNA of MCP-1 in the liver tissue of experimental group that curedby metformin,pioglitazone and JDTLTGS obviously decreased, which have remarkabledifference from the DM model group (P＜0.01). So it is the molecular mechanism that theexcess expression of NF-κB,MCP-1 in DM model group liver results from inflammatoryPathogenesis in liver. JDTLTGS can decrease the protein expression of NF-κB,MCP-1 and themRNA expression of MCP-1 in the liver tissue. JDTLTGS inhibitory effect on excessexpression of NF-κB,MCP-1 in DM model group liver, and inhibit the inflammatoryPathogenesis in liver, which is one of the function mechanisms that JDTLTGS capsuleprevent and treat T2DM,IR.3.4 The study about effect of JDTLTGS on the protein and gene expression pathway ofIRS-2 in experimental diabetic rat's liverIt was done that assaying the protein expression of IRS-2 in experimental rats' livertissue of each group by immunohistochemical method and the expressive content of IRS-2mRNA in experimental rats' liver tissue of each group by RT-PCR method and observingJDTLTGS's effect on IRS-2 in diabetic rats' liver, so that we could probe whether the mechanism of inflammatory Pathogenesis in liver leading to T2DM,IR is by affecting theexpression of IRS-2 in liver. The results showed: the protein expression of IRS-2 and the levelof IRS-2 mRNA in modal group obviously decreased more than normal control group(P＜0.01); the protein expression of IRS-2 and the gene expression of IRS-2 in the liver tissueof experimental group that cured by metformin and JDTLTGS obviously increased,whichhave remarkable difference from the DM model group (P＜0.01); while the experimental groupthat cured by pioglitazone has no change. It indicated that JDTLTGS could obviously increasethe expression of IRS-2 in diabetic rats' liver, which maybe partly had correlation with itsability to prevent and treat DM by intervening the way of NF-κB,MCP-1 and inhibiting theinflammatory pathogenesis in liver of T2DM,IR.JDTLTGS can increase the expression of IRS-2 in the experimental rats' liver on the baseof inhibiting the inflammatory pathogenesis in liver, besides whether it is other pathway andkey to improve insulin sensitivity,prevent and treat T2DM,IR,which we need study deeply.
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