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Atherosclerosis （AS） is a chronic inflammatory pathological process in which lipid and/or fibrous substances are deposited in the intima of arteries， and it is one of the pathological bases of many cardiovascular and cerebrovascular diseases. Endoplasmic reticulum stress （ERS） is a protective mechanism of cell adaptation. Moderate ERS can reduce abnormal protein aggregation and increase the degradation of misfolded proteins to repair and stabilize the internal environment， while excessive ERS can cause unfolded protein reaction， activate inflammation， oxidative stress， apoptosis， autophagy， and other downstream pathways， and lead to cell damage， or even apoptosis. A large number of studies have shown that ERS mediates a variety of pathological processes related to AS， affects endothelial cells， smooth muscle cells， macrophages， endothelial progenitor cells， and other cell components closely related to its occurrence and development， influences the progress of AS by regulating cell function， and promotes the formation of AS plaque， the transformation of stable plaque to unstable plaque， and the rupture of unstable plaque. Regulation of ERS may be a key target for the prevention and treatment of AS， and it is a research hotspot at present. Traditional Chinese medicine （TCM） believes that the origin of AS is the imbalance of Yin and Yang， the disharmony of Zangfu organs， and the abnormal operation of Qi， blood， and body fluid， which leads to the accumulation of phlegm， blood stasis， and other pathological products in the pulse channels， making the blood flow blocked or misfunction and causing the disease， which belongs to the syndrome of deficiency in origin and excess in superficiality. As the pathogenesis of AS is complex， and the symptoms are diverse， TCM has significant advantages in treating AS because of its multiple targets， multiple pathways， stable efficacy， strong individualization， and high safety. This paper systematically elaborated on the role of ERS in the occurrence and development of AS and summarized the mechanism research on the regulation and control of ERS by Chinese herbal monomer， Chinese herbal extract， Chinese herbal compound， and proprietary medicine， so as to provide a theoretical basis for clinical research and drug development in the prevention and treatment of AS.
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In western medicine， the small intestine anatomically belongs to the digestive system and is also an important immune organ of the body. The innate immune system of the small intestine consists of a tissue barrier， innate immune cells， and innate immune molecules. The dysfunction of any part can cause metabolic disorders and eventually lead to diabetes. In the pathogenesis of diabetes， traditional Chinese medicine （TCM） has the theory of ''spleen deficiency causing diabetes''， which points out that the impaired spleen function results in inadequate transformation， impaired essence spread， and turbidity by essence accumulation， which is the core pathological link of blood glucose metabolism disorder in diabetes. In terms of the relationship between the small intestine and the spleen， the theory of TCM holds that the small intestine is located in the abdomen and the abdomen is dominated by the spleen. The digestion， absorption， and endocrine functions of the small intestine are also similar to the functions of spleen in governing movement and transformation and spreading essence by virtue of spleen Qi. Therefore， the anatomical and physiological functions of the small intestine in western medicine are closely related to the spleen in TCM. At the same time， the spleen is closely related to the innate immune function of the small intestine in TCM. The spleen participates in the generation and distribution of defense Qi， and the process of defense Qi playing the external function is similar to the process of the activation of the innate immune response. The spleen is also an important organ involved in fluid metabolism， which can cooperate with the lung and kidney to timely remove turbid fluid from the body. It can also work with the stomach as the hub of Qi ascending and descending and regulate the physiological activities of "clear Yang" and "turbid Yin"， so as to ensure the homeostasis of the internal environment of the body， which is the basis for maintaining the normal function of the innate immunity of the small intestine. Therefore， taking "spleen deficiency causing diabetes" as a bridge， the theory of TCM and western medicine were combined to explain the relationship between small intestinal innate immunity imbalance and the pathogenesis of diabetes from the perspective of TCM， which is helpful to understand the pathogenesis of diabetes in a deeper level and also provide a new perspective and new way for the prevention and treatment of this disease with TCM.
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Diabetic cardiomyopathy （DCM） is one of the complications of diabetes. It refers to a specific type of idiopathic cardiomyopathy that occurs in individuals with diabetes， distinct from other cardiovascular diseases such as coronary heart disease， valvular heart disease， or congenital heart disease. It has also been identified as one of the leading causes of death in diabetic patients for many years. Research has shown that the pathogenesis of DCM is closely associated with insulin resistance， activation of various inflammatory responses， increased oxidative stress， impaired coronary microcirculation， and accumulation of advanced glycation end products （AGEs）. Among various inflammatory responses， the activation of the NOD-like receptor protein 3 （NLRP3） inflammasome can induce the secretion of a large amount of pro-inflammatory cytokines through the cascade reaction of inflammation， subsequently mediating cellular pyroptosis and promoting myocardial damage. Currently， extensive experimental studies on traditional Chinese medicine （TCM） have been conducted in China and abroad based on the significant role of the NLRP3 inflammasome in the prevention and treatment of DCM. These studies have demonstrated that Chinese medicinal extracts， such as Astragalus polysaccharide and ginsenoside Rb1， single drugs like Coriolus and Cordyceps， and Chinese medicinal formulas like Didangtang and modified Taohe Chengqitang， as well as acupuncture and TCM exercise therapy， can regulate the relevant pathways of the NLRP3 inflammasome to inhibit its assembly or activation， reduce inflammatory responses， inhibit myocardial remodeling in DCM， and improve cardiac function. This article reviewed the relationship between the NLRP3 inflammasome and DCM， as well as the research progress on TCM in exerting anti-inflammatory effects in this field， aiming to provide new insights for the development of therapeutic approaches for DCM.
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Objective:To analyze the distribution characteristics of traditional Chinese medicine (TCM) syndromes in patients with coronavirus disease 2019 (COVID-19) in plateau areas, and to provide theoretical basis for further clinical treatment of patients with COVID-19.Methods:From August 9 to August 24, 2022, patients with COVID-19 admitted to the Third People's Hospital of Tibet Autonomous Region (designated hospital for COVID-19) were included, and their baseline characteristics (age, gender, source), clinical classification and distribution of TCM syndrome types were collected and analyzed. Data analysis was performed using SPSS 26.0 statistical software.Results:A total of 161 COVID-19 patients were enrolled with ethnic distribution: 124 (77.02%) Tibetans, 35 (21.74%) Han, and 2 (1.24%) Hui, 68 males and 93 females. The male-to-female ratio was 0.73∶1. Aged 1 to 94 years, the average age was (39.06±23.64) years old, of which 4 patients were under 1 year old (excluded because the information was missing). A total of 157 patients were enrolled, and 124 patients (78.9%) were under 60 years old, including 120 cases of common type, 4 cases of severe type, 0 cases of critical type, 7 cases over 80 years old, 1 case over 90 years old, and 32 cases under 18 years old. The clinical manifestations of the patient are mainly cough, expectoration, fever, aversion to cold, dry throat, headache, fatigue, running nose, dry mouth, bitter mouth, etc. Most of the tongue is pale, red, and white greasy moss or thin white coating. In TCM, the most common syndrome was cold-dampness blocking lung syndrome (99 cases, 63.06%), followed by cold-dampness stagnant lung syndrome (22 cases, 14.01%), damp-heat accumulating lung syndrome (22 cases, 14.01%), and humidity stagnant lung syndrome (11 cases, 7.01%). Syndromes of epidemic (2 cases, 1.27%), epidemic toxins blocking the lung pattern (1 cases, 0.64%), toxins with dryness intense heat in both qi and ying phases pattern (0 cases) accounted for less than 2%, and the distribution of various syndrome types in COVID-19 patients was uneven ( χ2 = 0.48, P < 0.05). Conclusion:The most common TCM syndromes of COVID-19 patients in Lhasa are cold-dampness blocking lung syndrome, followed by cold-dampness stagnant lung syndrome, damp-heat accumulating lung syndrome, and humidity stagnant lung syndrome.
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The basic pathological change of diabetic macroangiopathy is atherosclerosis， and the metabolism legacy effect of hyperglycemia will cause continuous damage to the large vessels. Oxidative stress is a common mechanism for diabetes and its chronic complications and it is also the basis of the metabolism legacy effect which keeps damaging the large vessels. Anti-oxidant therapy can delay the course of diabetic macroangiopathy. According to the theory of traditional Chinese medicine （TCM）， the pathogenicity of hidden pathogen is concealing， lingering， and refractory. On the basis of the syndrome and treatment of collateral diseases， vessel-collateral theory， and hidden pathogen theory of TCM， the pathological changes of diabetic macroangiopathy are summarized as pathogen concealment-accumulation of sugar and lipids leading to phlegm and blood stasis-accumulation of toxins-damage to vessels and collaterals-hardening vessels. The core pathogenesis is the hidden pathogen damaging the collaterals， and the basic pathological change is vessel hardening. The toxins of sugar， lipid， phlegm， and stasis are the pathological products and the key to be treated. According to this theory， the medicinal materials with the functions of activating blood to dredging collaterals， resolving phlegm to clearing collaterals， Promoting qi to unblocking collaterals and removing toxins to shunting collaterals can be selected for prescription. These medicinal materials can inhibit the generation of reactive oxygen species， affect the oxidase activity， and enhance the antioxidant capacity， thereby regulating the oxidative stress response， protecting the vascular endothelial function， reducing the damage of the large blood vessels， and slowing down the progression of the disease. Such therapy is of great significance in clinical practice and research， providing a new idea for the prevention and treatment of diabetic macroangiopathy.
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Exercise plays a critical role in non-drug treatment of diabetes .However,exercise-associated hypoglycemia (EAH) restrains diabetic patients from exercising .Till now,the underlying mechanism of exercise-associated hypoglycemia is unclear .Here we reviewed studies on pathogenesis of exercise-associated hypoglycemia in diabetes,in order to provide references and ideas for further studies in EAH .
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The academic origin of homogeny of spleen and pancreas is explained from the aspect of Chinese medicine.The authors think spleen faihng to spread essence is the basic pathogenesis to diabetes mellitus.Spleen function of spreading essence is impaired.Thus essence of water and grain could not be spread in the whole body but amass sugar-turbidity,which manifests high blood sugar.Differentiating diabetes mellitus from the viewpoint of spleen,invigorating spleen and benefiting Qi could help spleen to ascend clear.Invigorating spleen-yin and clearing endogenous heat are used.The liver and kidney should be considered.The methods of dissipating phlegm and activating blood circulation could be combined.The treating idea of treating spleen is treating pancreas should be used in preventing and treating diabetes mellitus.
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Objective To explore the effect of Shenqi Fufang (参芪复方,SF) on skeletal muscle damage of type 2 diabetes mellitus (T2DM) and its possible mechanism.Methods Eighteen rats with spontaneous type 2 diabetes mellitus (GK) were randomized into the model group,SF group and sitagliptin group with six rats in each group,and six more Wistar rats were selected as the control group.Each group was given high fat diet for 8 weeks to build T2DM model except for the control group.At the same time,the control group and the model group were given normal saline 5 ml/(kg-d) by gastric perfusion,the SF group was given SF extract 1.44g/(kg · d) by gastric perfusion,and sitagliptin group was given sitagliptin phosphate suspension 16ml/(kg · d) by gastric perfusion.Eight weeks later,the levels of serum insulin-like growth factor 1 (IGF-1),tumor necrosis factor-αr (TNF-a) and interleukin-1β (IL-1β)were measured in each group,the gastrocnemius muscle was taken out to get the wet weight and observe the pathological changes,and the expression of p70s6k1 protein was detected.Results Compared with the control group,the wet weight of the gastrocnemius muscle,the serum IGF-1 level and p70s6k1 protein expression in the model group significantly decreased (P ＜ 0.05),while the levels of serum TNF-α and IL-1β significantly increased (P ＜ 0.05).Through pathological observation,there existed gastrocnemius muscle cells atrophy,a larger area of edema and interstitial lymphocyte infiltration.Compared with the model group,the wet weight of the gastrocnemius muscle,IGF-1 content and p70s6k protein expression in the sitagliptin group and the SF group significantly increased,the contents of TNF-α and IL-l β significantly decreased (P ＜0.05),and there were no obvious muscle cell atrophy and edema,and also little inflammatory cell infiltration.There was no significant difference between the sitagliptin group and SF group (P ＞ 0.05).Conclusion SF could reduce the diabetic skeletal muscle injury;the potential mechanism seems to reduce the inflammatory factor content,improve IGF-1 resistance and maintain the skeletal muscle mass.
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Objective To investigate the effect of Tongluo Tangtai Recipe(TTR)on inflammatory cytokines in rats with diabetic peripheral neuropathy(DPN). Methods Rat model of spontaneous DPN was established by feeding high fat diet. The rats were divided into 5 groups , namely model group , western medicine(metformin 100 mg·kg-1·d-1+ methycobal 0.2 mg·kg-1·d-1) group, and low-, middle- and high-dose TTR groups (TTR in the dosage of 0.72, 1.44, 2.88 g·kg-1·d-1 respectively). Rats of the normal group and model group were treated with normal saline orally, and the medication groups were given the corresponding medicine according to the experimental design. After intragastric administration for 4 weeks, sciatic motor/sensory nerve conduction velocity was detected with electrophysiological examination method, and tumor necrosis factor alpha(TNF-α), interleukin-6(IL-6), C-reactive protein(CRP), myelin basic protein(MBP) levels in the serum were examined by enzyme-linked immunosorbent assay(ELISA). Results TTR in various dosages could reduce the serum levels of MBP and inflammatory cytokines of TNF-α, IL-6 and CRP, and increase sciatic nerve conduction velocity (P<0.05 or P<0.01 compared with those in the model group), the high dose showing the strongest effect. Conclusion TTR could inhibit inflammation reaction and nerve demyelination, and improve nerve structure and conduction function, which may contribute to the preventive and therapeutic mechanism of TTR for DPN.
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Objective To establish a simple diabetic peripheral neuropathy (DPN) rat model with the high fat-fed in GK rats. Methods A total of 30 GK rats (7-8 weeks) were fed with high-fat diet to establish the DPN model. Thirty normal Wistar rats were fed with ordinary diet (control group). The blood-sugar value, body mass, water-intake and food-intake were monitored every week in two groups. The serum level of glycosylated hemoglobin, the right sciatic nerve conduction velocity were detected at 8, 12 and 16 weeks respectively. The left sciatic nerve was used for HE and TUNEL staining. Results The manifestations of polydipsia, polyphagia and growth retardation were gradually appeared in GK rats. After 12 and 16 weeks, the blood-sugar and glycosylated hemoglobin were significantly increased in GK rats compared with those of normal Wistar rats (P 0.05). The sciatic nerve pathological features and Schwann cell apoptosis suggested that the model of DPN was successfully established (apoptosis index, P <0.01). Conclusion GK rats fed by high-fat diet are the satisfactory models of the DPN in experimental research. And 12-week is a suitable and economical time for molding.
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[Objective]To investigate the mechanism of Qingre Yiqi Tongluo(QRYQTL) fang in treating the diabetic nephropathy. [Methods]60 Sprague-Dawleg rats were divided into normal control group(N), Diabetic nephropathy model group(M) (model rats were prepared by intraperitoneal injection with STZ after unilateral nephrectomy), then the model rats were assigned into model control group, QRYQTL fang treatment group(Q) and Irbesartan treatment group(I). After 12 weeks of the treatment, the contents of superoxide dismutase(SOD),catalase(CAT),glutathione peroxidase(GSH-Px) and malondialdehyde (MDA) in renal tissue were examined by enzyme linked immunoassay(ELISA); the glomerular area(GA), mesangium area(MA),MA/GA, mean width of the podocyte foot processes(FPW) ,foot process fusion rate(FPFR) and average thickness of glomerular basement membrane(GBMT) were measured. [Results]Compared with N group, the contents of MDA in kidney homogenate and the GA,MA, FPW,FPFR,GBMT were markedly increased (P<0.01or P<0.05),the contents of SOD,CAT, GSH-Px and MA/GA were significantly decreased( P<0.01or P<0.05). QRYQTL fang reduced the level of MDA and decreased the GA, FPW, FPFR and GBMT(P<0.01or P<0.05). Compared with I group ,the QRYQTL fang was superior to Irbesartan in reducing the MDA, FPFR as wel as increasing the SOD,CAT(P<0.05).[ Conclusions]QRYQTL fang has a protective effect on the experimental diabec-tic nephropathy rats. The mechanism may be related to inhibiting oxidative stress, improving the body ’s antioxidant ability and al eviating the glomerular morphologic injury.
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Objective To investigate the correlation of diabetic skeletal muscle disease with macroangiopathy, and to explore the related genes of Shenqi Compound Recipe (SCR) in preventing and treating diabetic skeletal muscle disease by using gene chip technique, thus to reveal the molecular mechanism. Methods KKAy mice were fed with water containing nitri oxide synthase inhibitor of Nω-nitro-L-arginine methyl ester ( L-NAME) and high fat diet to induce the macroangiopathy complicated with type 2 diabetes. The experimental animals were divided into normal c57BL/GJ group, KKAy group, model group, SCR group (in the dosage of 14.4 g·kg-1·d-1) and rosiglitazone group ( in the dosage of 1.33 mg·kg-1·d-1) , 15 in each group. The medication groups were administered the corresponding agents for 8 consecutive weeks just as the modeling began. During the experiment period, blood glucose was monitored. At the end of the experiment, the abdominal aorta and skeletal muscle of mice were taken out for the observation of morphological changes, and differentially expressed genes of skeletal muscle between SCR group and model group, and between model group and KKAy group were detected by gene chip technique. Results SCR had an effect on relieving the atrophy, edema, fracture, and inflammatory changes in the skeletal muscle. There were 198 genes differentially expressed between model group and KKAy group, including 119 up-regulated genes and 79 down-regulated genes. There were 70 genes differentially expressed between SCR group and model group, including 33 up-regulated genes and 37 down-regulated genes. In the two comparison groups, 7 genes ( Celsr2, Rilpl1, Dlx6as, 2010004M13Rik, Anapc13, Gm6097, Ddx39b) showed reversed differential expression. Conclusion Diabetic skeletal muscle disease is associated with macroangiopathy. SCR has preventive effect on diabetic skeletal muscle lesion, and the mechanism may be related to the regulation of Celsr2, Rilpl1, Dlx6as, 2010004M13Rik, Anapc13, Gm6097, Ddx39b gene expression.
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[Objective]To study the effect of Qingre Yiqi Tongluo(QRYQTL) preseription on proteinria in diabetic nephropathy(DN) rats by means of ob-servation on the expressions of fibroblast-specific protein 1(FSP1) and P-cadherin in in glomerulus in rats.[Methods]60 Sprague-Dawleg rats were divided into normal control group(N), Diabetic nephropathy model group(M), QRYQTL preseription treatment group(Q) and Irbesartan treatment group(I). DN model rats were prepared by intraperitoneal injection with STZ after unilateral nephrectomy. The rats were sacrificed after 12 weeks of the treatment. The creatinine clearance(Ccr),blood urea nitrogen(BUN) and 24h urinary protein(UPro) were tested. Immunohistochemical staining was performed to explore the expressions of P-cadherin and fsp1 in glomerulus.[Results] ①Compared with M group, the levels of 24-hour upro in Q group were significantly de-creased(P<0.01).The levels of Ccr and BUN in Q group were both lower than those of M group( P<0.05). ② Compared with M group, the expressions of P-cadherin in glomerulus in Q group were increased( P<0.01) and the expressions of FSP1 were obviously decreased( P<0.01). The expressions of FSP1 in Q group were decreased compared with that of I groups(P<0.05).[Conclusions]QRYQTL preseription weakened the epithelial-mesenchymal transition (EMT) of podocyte by means of increasing the expression of P-cadherin and reducing the expression of FSP1, thereby decreased the Upro and protect the renal function.
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Objective:To explore the effects of Shenqi Compound Recipe on the expression of Cycloxygenase-2 (COX-2)mRNA in aorta in GK rats.There were five groups:GK group,model group,atorvastatin group,Shenqi Compound Recipe group and normal control group.During the experiment periods,each group was administrated correspondent substance respectively for 35 days.Serum concentrations of C reactive protein(CRP)were determined by ELISA.The mRNA expressions of COX-2 in aorta were detemined by reverse transcriptase PCR(RT-PCR).Results:Compared with model group,concentrations of CRP in serum and the mRNA expression of COX-2 all decreased in atorvastatin group and Shenqi Compound Recipe group(P
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Objective: To explore the mechanism of ShenQi compound recipe on preserving vessel endothelium with type 2 diabetes mellitus(T2DM) macroangiopathy in GK rats.Methods: GK rats were randomly divided into Ramipril group,ShenQi compound recipe low dosage group,ShenQi compound recipe high dosage group and Wistar control group.Each group was administrated correspondent substance respectively for 28 days after intra-peritoneal injection of L-NAME and administration of high fat diet for 2 weeks except Wistar control group.To determine ICAM1 by ELISA,ET-1 by radioimmunassay,NOS by chemical shade selection,NO by nitrate reductase method,mRNA expression of ICAM-1 in aorta by real time RT-PCR. Results: Compared with model group,the contents of NO,NOS increased,the ET1 and the expression of thoracic aorta ICAM-1mRNA decreased remarkably in ShenQi compound recipe group(P
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Objective To observe the effect of ligustrazine (TMP) on the expression of connective tissue growth factor (CTGF) and osteopontin (OPN) in the renal tubulointerstitium of diabetic nephropathy (DN) rats. Methods Wistar rats were used to establish the models through intraperitoneal injection of onedose streptozotocin (STZ) and nephrectomy. Rats were divided into 5 groups at random: model group, blank control group, Lotensin (1.7 mg? kg- 1? d- 1) group, of high-and lowdosage of TMP groups (150, 50 mg? kg- 1? d- 1). Except the rats in blank group and model group, the rats received corresponding medicines according to the experimental design for 12 weeks.Volume of urine protein within 24 hours was examined in the 4th, the 8th and the 12 th week, OPN mRNA expression in the renal tubulointerstitium was detected by RT- PCR and CTGF was detected by means of immunohistochemistry. Results Compared with normal group, the volume of 24 h urine protein rised obviously (P