THE PROTECTIVE EFFECT OF FASCIOTOMY COMBINED WITH HYPERTONIC SALINE FLUSHING FOR CRUSH SYNDROME IN RATS.

Crush injury and syndrome: A review for emergency clinicians

Previously we showed that Ani (anisodamine)/Neo (neostigmine) combination produced anti-shock effect via activating α7 nicotinic acetylcholine receptor (α7nAChR). In this study, we aim to investigate the therapeutic effect and underlying mechanisms of Ani/Neo combination in acute lethal crush syndrome (CS). In rat and rabbit CS models, Ani/Neo combination increased the 24 h survival rates, improved hemodynamics and decreased the levels of creatine kinase, MB isoenzyme of creatine kinase, blood urea nitrogen, creatinine, K+ in serum. It also decreased the levels of H2O2, myeloperoxidase (MPO) and nitric oxide (NO) in serum and compressed muscle in rat CS model. In wild-type (WT) mice with CS, Ani/Neo combination increased 24 h survival rate and decreased the levels of H2O2, MPO, NO, TNFα, IL-6 and IL-10 in compressed muscle. These effects were attenuated by α7nAChR knockout (KO). Moreover, Ani/Neo combination prevented the decrease of phosphorylation of Janus kinase 2 (JAK2) and phosphorylation of signal transducer and activator of transcription 3 (STAT3) induced by CS. These effects of Ani/Neo in CS mice were cancelled by methyllycaconitine (α7nAChR antagonist) and α7nAChR KO. Collectively, our results demonstrate that Ani/Neo combination could produce therapeutic effects in CS. The underlying mechanism involves the activation of α7nAChR-dependent JAK2-STAT3 signaling pathway.

Crush syndrome (CS) is characterized by ischemia/reperfusion-induced rhabdomyolysis and the subsequent onset of systemic inflammation. CS is associated with a high mortality, even when patients are treated with conventional therapy. We hypothesized that treatment of lethal CS rat model with dexamethasone (DEX) have therapeutic effects on the laboratory findings and clinical course and outcome. To create a CS model, anesthetized rats were subjected to bilateral hind limb compression with rubber tourniquets for 5 hours and randomly divided into three groups as follows: saline-treated CS group, CS groups treated with low (0.1 mg/kg) and high doses (5.0 mg/kg) of DEX. Saline for the CS group or DEX for the DEX-treated CS groups was intravenously administered immediately before reperfusion. Under continuous monitoring and recording of arterial blood pressures, blood and tissue samples were collected for histologic and biochemical analysis at designated period before and after reperfusion. Ischemic compression of rat hind limbs reduced the nitrite content in the crushed muscle, and the subsequent reperfusion induced reactive oxygen species-mediated circulatory collapse and systemic inflammation, finally resulting in a mortality rate of 76% by 48 hours after reperfusion. A single injection of high-dose DEX immediately before reperfusion activated endothelial nitric oxide synthase (eNOS) by sequential phosphorylation through the nongenomic phosphoinositide 3-kinase (PI3K)-Akt-eNOS signaling pathway. DEX also exhibited anti-inflammatory effects by modulating proinflammatory and anti-inflammatory mediators, consequently suppressing myeloperoxidase activities and subsequent systemic inflammation, showing a complete recovery of the rats from lethal CS. These results indicate that high-dose DEX reduces systemic inflammation and contributes to the improved survival rate in a rat CS model.

Earthquakes are major causes of morbidity and mortality. The Wenchuan region of China was devastated by a catastrophic earthquake on May 12, 2008, at 02:28 p.m. (Beijing time), registering magnitude 8.0 on the Richter scale and causing more than 69,181 deaths. As a first-line general hospital in the disaster area, Mianyang Central Hospital admitted a large number of the victims. A total of 534 victims (246 males, 288 females) were categorized as non-crush injury patients (n=239), simple crush injury patients (n=136), and crush syndrome patients (n=69) according to their traumatic conditions. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), cholinesterase (CHS), and creatine kinase (CK) levels were measured. ALT, AST, LDH, CHS, and CK levels showed significant differences among the three groups by one-way analysis of variance (ANOVA). Pearson correlation analysis showed that correlative changes between any two of the following: ALT, AST, GGT, ALP, LDH, and CHS were similar among three groups, with the following exceptions. The correlation coefficients of ALT-GGT, AST-GGT, and ALP-CHS changed from positive to negative values, and ALP-LDH changed from a negative value to a positive value. Receiver-operating characteristic (ROC) curve analysis showed the highest diagnostic effectiveness of 99.4% for CK, with 100% specificity [positive predictive value (PPV)=100%] and 99.4% sensitivity [negative predictive value (NPV)=99.0%] in distinguishing crush injury (including crush syndrome) from non-crush injury. AST had the best diagnostic effectiveness in distinguishing crush syndrome from crush injury; 53.8%, with 85.5% specificity (PPV=64.4%) and 77.9% sensitivity (NPV=90.7%). Multivariate logistic analysis revealed that CK was best at distinguishing crush injury (including crush syndrome) from non-crush injury (OR 409.636, 95% CI 382.96-438.17), and AST was best for distinguishing crush syndrome from crush injury (OR 50.08, 95% CI 46.84-53.55). Crush injury and crush syndrome are severe in victims following accidents or natural catastrophes. Serum CK, LDH, AST, ALT, GGT, and ALP activities were all helpful biochemical parameters in estimating the severity of crush injury and/or crush syndrome and preventing the development of further complications.

To study the protective effects and related mechanism of bicyclol on liver fibrosis induced by carbon tetrachloride (CCl(4)). Forty male Wistar rats were injected subcutaneously with 25% CCl(4) twice a week for 3 months. Since the 7th week the rats were divided into 4 groups of 10 rats: normal control group, CCl(4) model group, bicyclol 100 mg/kg group (perfused of bicyclol into stomach 100 mg/kg qd for 45 days), and bicyclol 200 mg/kg group (perfused of bicyclol into stomach 200 mg/kg qd for 45 days). Twenty-four hours after the last administration the rats were killed. The serum was isolated to measure the levels of alanine transaminase (ALT), aspartate aminotransferase (AST), total bilirubin (TB), albumin/globulin (A/G), total protein (TP), hyaluronic acid (HA), and pro-collagen peptide III (PIIIP). Serum TNF alpha content was examined by ELISA assay, and liver TGF beta 1 level was determined by immunohistologic assay. The pathology of liver was examined. Twenty-eight mice were divided into 4 groups of 7 mice: normal control group, subacute group, 100 mg bicyclol group (perfused of bicyclol into stomach 50 mg/kg bid), and bicyclol 200 mg/kg group (perfused of bicyclol into stomach, 100 mg/kg bid), and 200 mg bicyclol group. Carbon tetrachloride was injected subcutaneously to the mice in the latter 3 groups every 3 days for 1 month. Twenty-four hours after the last administration the mice were killed and the serum was isolated to measure the levels of ALT, AST, TP, and albumin. Mitochondria were extracted from the livers of the experimental animals to measure the amount of protein. Mitochondrial glutathione (GSH) and malondialdehyde (MDA) contents were measured. The MDA and GSH contents in the control group were regarded as 100%, and the percentages of MDA and GSH in other groups were calculated. The fluidity of mitochondrial membrane and swelling degree of mitochondria were measured. Imunohistochemistry was used to detect the liver TGF beta 1. Nuclear NF kappa B DNA binding activity was investigated by electrophoretic mobility shift assay. Three months after the administration of carbon tetrachloride the serum ALT, AST, TB, HA, and PIIIP levels of the CCl(4) model group increased by 24, 10, 8, 28, and 4 times and the levels of albumin and A/G decreased significantly in comparison with those of the normal control group. However, the serum ALT, AST, TB, HA, and PIIIP levels in the 2 bicyclol groups were significantly lower than those in the model group. The pathological changes in the liver of the 2 bicyclol groups were significantly lighter than those in the model group. The serum TNF alpha increased significantly in the model group, however, the serum TNF alpha levels in the 2 bicyclol groups were significantly lower than that of the model group. The liver TGF beta 1 level in the model group was 4 times that of the normal control group. The liver TGF beta 1 level in the 2 bicyclol groups were significantly lower than that of the model group. One month after the administration of carbon tetrachloride to mice the serum ALT and AST increased and A/G decreased significantly. However, in the 2 bicyclol groups the serum ALT and AST were significantly lower and the A/G ratio was significantly higher in comparison with the model group. The mitochondrial GSH decreased by 34% and the mitochondrial MDA increased by 60% in the model group. The mitochondrial GSH was normal in the 2 bicyclol groups and the MDA level was significantly lower than that of the model group. The fluidity and swelling ability of mitochondrial membrane significantly decreased in the model group mice and the fluidity and swelling ability of mitochondrial membrane in the 2 bicyclol group mice were relatively normal. Twelve and twenty-four hours after the damage by carbon tetrachloride the binding activity of nuclear NF kappa B remained very high in the model group mice and was significantly lower in the 2 bicyclol group mice in comparison with the model mice. Bicyclol alleviates CCl(4)-induced liver fibrosis by its anti-peroxidation and anti-inflammation functions and regulation of NF-kappa B DNA-binding activity.

Crush syndrome (CS) is a serious medical condition characterized by muscle cell damage resulting from pressure. CS has a high mortality, even when patients receive fluid therapy. We examined whether administration of NaNO2-containing fluid can improve survival in a rat model of CS. The CS model was generated by subjecting anesthetized rats to bilateral hind limb compression with a rubber tourniquet for 5 h. Rats were then randomly divided into six groups: sham; CS with no treatment; CS with normal saline treatment; CS with normal saline + 25 mEq/L bicarbonate treatment; and CS with normal saline + 200 or 500 μmol/kg NaNO2. Blood and tissue samples were collected for histological and biochemical analyses at predetermined time points before and after reperfusion. Ischemic compression of rat hind limbs reduced nitrite content in the crushed muscle, and subsequent reperfusion resulted in reactive oxygen species-induced circulatory dysfunction and systemic inflammation. Rats treated with 200 μmol/kg NaNO2 showed increased nitric oxide (NO) levels, blood circulation, and neoangiogenesis, decreased generation of reactive oxygen species, and suppression of the inflammatory response, leading to complete recovery. Treatment with 200 μmol/kg NaNO2 prevents muscle damage induced by ischemia reperfusion via the protective effects of NO and suppression of systemic inflammation, thereby increasing survival rates in CS.

Crush syndrome (CS) is a potentially lethal condition characterized by muscle cell damage resulting from decompression following compression. Patients with CS can develop cardiac failure, kidney dysfunction, shock, systemic inflammation and sepsis. Salvianolic acid B (SalB) has cardiac and kidney protective effects and anti-oxidative, anti-inflammatory, anti-apoptotic and anti-bacterial properties. The present study aimed to demonstrate the survival benefit of SalB in the CS rat model, which comprised anesthetized rats with bilateral hindlimb compression by a rubber tourniquet for 5 h. The rats examined were randomly divided into four groups: i) Sham; ii) sham treated with SalB; iii) CS rat model without treatment; and iv) CS rat model treated with SalB. Under continuous monitoring and recording of arterial blood pressures, blood and tissue samples were collected for biochemical analyses at designated timepoints before and after reperfusion. SalB administration improved the survival rate, kidney function (by treating shock and metabolic acidosis) and inflammation (by reducing mitochondrial dysfunction and endothelial damage). Reduced incidence of cardiac failure due to hyperkalemia was associated with reduced muscle injury via the prevention of mitochondrial dysfunction. Additionally, indirect antibacterial action by the neutrophil extracellular trap system (NETs) was observed. SalB administration to the CS rat model led to a substantial improvement in survival following CS by decreasing kidney and cardiac dysfunctions, inflammation, and endothelial dysfunction by improving the mitochondrial function and through antibacterial effects via NETs.

Nitrite is an intrinsic signaling molecule with potential therapeutic implications in mammalian ischemia/reperfusion (I/R) injury of the heart, liver, and kidney. Although limb muscle compression and subsequent reperfusion are the causative factors in developing crush syndrome (CS), there has been no report evaluating the therapeutic effects of nitrite on CS. We therefore tested whether nitrite could be a therapeutic agent for the treatment of CS. To create a CS model, anesthetized rats were subjected to bilateral hind limb compression with rubber tourniquets for 5 hours, followed by reperfusion for 0 hour to 6 hours while monitoring blood pressure. Saline for the CS group or sodium nitrite (NaNO(2)-100, 200, and 500 μmol/kg) for the nitrite-treated CS groups was intravenously administered immediately before reperfusion. Blood and tissue samples were collected for biochemical analysis. Tissue nitrite levels in injured muscles were significantly reduced in the CS group compared with the sham group during I/R injury. Nitrite administration to CS rats restored nitric oxide bioavailability by enhancing nitrite levels of the muscle, resulting in a reduction of rhabdomyolysis markers such as potassium, lactate dehydrogenase, and creatine phosphokinase. Nitrite treatment also reduced plasma levels of interleukin-6 and myeloperoxidase activities in muscle and lung tissues, finally resulting in a dose-dependent improvement of survival rate from 24% (CS group) to 36% (NaNO(2)-100 group) and 64% (NaNO(2)-200 and 500 groups). These results indicate that nitrite reduces I/R-induced muscle damage through its cytoprotective action and contributes to improved survival rate in a rat CS model.

Natural disasters cause enormous environmental, economic, and human losses. Children are the most vulnerable group and face severe consequences. While the primary cause of post-traumatic death is direct injury, the secondary cause is crush syndrome (CS). In this study, we aimed to share our experience in the management of children with CS during disasters by evaluating the clinical and laboratory outcomes of a group of 26 paediatric patients. Age, weight, length of time under rubble, laboratory results, and characteristics of crush injuries were assessed in 26 paediatric patients admitted to the emergency department after the earthquake. Diagnostic criteria for CS were established and the need for dialysis, hyperbaric oxygen or amputation and its determinants were assessed. Crush syndrome was observed in 10 of the 26 patients. Significant differences in creatinine, aspartate aminotransferase, alanine aminotransferase, creatine kinase, hematocrit, pH, HCO3, and myoglobin levels were observed between patients with and without CS. None of the individuals rescued from the rubble within the first 6 hours had symptoms associated with CS. These 10 patients who developed CS were rescued within the first 48 hours of the earthquake, while 2 siblings were rescued after 81 hours and did not develop CS. The fact that the children were rescued from the rubble after 81 hours without developing CS shows the importance of patience in rescue operations. In addition, the very cold weather conditions during this earthquake may have prevented the development of dehydration and acute kidney injury and reduced the possibility of CS.

Effects of the mixture of Swertia pseudochinensis Hara and Silybum marianum Gaertn extracts on CCl4-induced liver injury in rats with non-alcoholic fatty liver disease

To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats. Male Wister rats were randomly divided into sham operation group (SOG), CS groups (CS6G, CS12G and CS24G) and tempol treatment group (TG, a ROS scavenger). CS model rats were established by crushing the hind limbs of rats with 15 kg pressure for 6 hours, and inferior caval vein blood and kidney samples were harvested at 6, 12, 24 hours after removing crush pressure. In TG, 100 mg/kg tempol was intraperitoneally injected into CS model rats after withdraw of crush pressure. In SOG, rats were fixed on the board without any crush pressure. The activation of c-jun was determined by western blotting. Serological parameters and the content of malondialdehyde (MDA) in kidney tissues were determined by standard methods. Acute kidney injury reached the peak at 12 hours after the crush pressure. Compared with SOG, the content of phosphorylated c-jun was significantly higher in CSG and TG (p < 0.05), and the content of phosphorylated c-jun in the CSG was significantly higher than that in TG (p < 0.05). Interestingly, the changes of the MDA content in the kidney tissues of the 3 groups were similar to the changes of phosphorylated c-jun content. ROS-mediated phosphorylation of c-jun may play important roles in the acute kidney injury of CS rats. Tempol can inhibit the phosphorylation of c-jun and alleviate the acute kidney injury.

Crush syndrome (CS) is characterized by ischemia/reperfusion-induced rhabdomyolysis and subsequent systemic inflammation and has a high mortality rate, even when treated with conventional therapy. In previous studies, we demonstrated that treatment of rats with acute lethal CS using dexamethasone (DEX) had therapeutic effects in laboratory findings and improved the clinical course of CS. However, because the application of DEX in CS therapy is unknown, evaluation of the pharmacokinetic parameters of DEX was considered essential to support its clinical use. Here, we investigated the pharmacokinetic characteristics of DEX in a rat model of CS. Anesthetized rats were subjected to bilateral hind limb compression using rubber tourniquets for 5 h, followed by reperfusion for 0 to 24 h. Rats were divided randomly into 4 groups: saline-treated sham (S) and CS groups and 5.0 mg/kg DEX-treated S (S-DEX) and CS (CS-DEX) groups. Blood and tissue samples were collected for HPLC analysis. In the CS-DEX group, the pharmacokinetic parameters of the area under the concentration-time curve, mean residence time, and distribution volume levels increased significantly compared to the S-DEX group, whereas total body clearance, elimination rate constant, and renal clearance levels decreased significantly. Moreover, decrease of muscle tissue DEX concentration and of CYP3A activity were observed in the CS-DEX group. These results show the pharmacokinetic characteristics of DEX in the rat CS model and support the potential use of DEX in disaster medical care.

To observe the effect of different core temperatures (Tc) after heat strike on serum inflammatory cytokines and multiple organ dysfunction syndrome (MODS) in rat. 120 male Sprague-Dawley (SD) rats were randomly divided into normal control group (n = 30) and heat strike group (n = 90). The rats in heat strike group were put into simulated thermal climate animal module after adaptive training. The module temperature was raised to 39 centigrade in 30 minutes with 65% humidity. The rats ran simultaneously at 15 m/min, on the slope of 0 degree angle, 8 minutes each time, 2 minutes interval, and the heat strike time was 90 minutes. After the rats came out of the module, rectal temperature, which was Tc value, was recorded. The rats died or Tc < 41 centigrade during the experiment were excluded, the remaining 73 rats were divided into three subgroups: 41.0-41.9 centigrade (n = 38), 42.0-42.9 centigrade (n = 26), and ≥43.0 centigrade (n = 9). The rats in the normal control group were reared at temperature of (25±2) centigrade, and humidity of (55±5)%. At 0 hour and 24 hours after the rats came out of the module, femoral artery blood was collected to determine serum interleukins (IL-1α, IL-1β, IL-17), tumor necrosis factor-α(TNF-α) andγ-interferon (IFN-γ) by enzyme-linked immunosorbent assay (ELISA). The cardiac troponin I (cTnI), MB isoenzyme of creatine kinase (CK-MB), serum creatinine (SCr), blood urea nitrogen (BUN), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were determined by automatic biochemical analyzer. The incidence of MODS and the number of accumulative organs within 24 hours of the rats in different Tc of heat strike group were compared and analyzed. The serum inflammatory cytokines and biochemical parameters at 0 hour after heat strike were significant higher than those of the normal control group, and showed a time dependence. Further analysis showed that the inflammatory response and organ dysfunction in rats were increased gradually with the increase in Tc of rats. Compared with the normal control group, at 24 hours after heat strike, inflammatory cytokines in Tc≥43.0 centigrade rats were increased obviously [IL-1α (ng/L): 13.56±2.07 vs. 2.24±0.62, IL-1β (ng/L): 17.11±1.90 vs. 7.40±1.52, IL-17 (ng/L): 17.00±1.41 vs. 6.00±1.78, TNF-α (ng/L): 16.78±1.79 vs. 7.27±1.74, IFN-γ (ng/L): 21.11±2.09 vs. 10.43±2.31], and the biochemical parameters were also increased obviously [cTnI (ng/L): 50.78±6.67 vs. 20.53±3.09, CK-MB (U/L): 62.89±3.82 vs. 22.00±3.01, SCr (μmol/L): 149.22±4.35 vs. 92.53±8.32, BUN (nmol/L): 55.22±1.99 vs. 19.10±2.02, ALT (U/L): 388.33±4.97 vs. 100.23±10.61, AST (U/L): 361.22±6.53 vs. 97.67±10.54, all P < 0.01]. The incidence of MODS within 24 hours in the heat strike group was 54.79% (40/73), and the higher the Tc, the higher the incidence of MODS, and the more insulted organs [the incidence of MODS in 41.0-41.9 centigrade, 42.0-42.9 centigrade, and ≥43.0 centigrade subgroups was 36.84% (14/38), 65.38% (17/26), 100.00% (9/9), and the organ involvement rate was 12.17% (37/304), 23.08% (48/208), and 48.61% (35/72), respectively, when 8 organs or systems were calculated for each rat, both P < 0.01]. The higher the Tc of heat strike rats, the stronger the inflammatory reaction and the more serious the damage of tissue, and the more extensive damage of the organs.

Crush syndrome is a severe systemic manifestation resulting from the breakdown of muscle cells leading to the release of toxic substances into the bloodstream. This condition can occur when a part of the body experiences a significant amount of pressure for an extended period. Crush syndrome presents with severe metabolic disruptions such as acute kidney injury, electrolyte disturbances, and cardiovascular collapse. It is essential to understand the pathophysiology and clinical features of crush syndrome for effective management and prevention of potentially devastating outcomes. The act of crushing and rupturing muscular cells generates a mechanical force that triggers the discharge of myoglobin. Subsequently, myoglobin undergoes a conversion into metmyoglobin and acid hematin, which are subsequently released into the systemic circulation. The muscular tissue harbors a variety of electrolytes and enzymes, which may attain toxic levels upon entry into the circulation in excessive quantities. The release of sodium, calcium, and fluids due to regional ischemia leads to increased muscle volume and tension, depletion of creatine kinase (CK) and ATP, and muscle vasodilation, further exacerbating hypotension. Crush syndrome can also lead to cardiovascular instability and renal failure due to vasomotor and nephrotoxic factors. Elevations in serum CK levels exceeding 1000 IU/l, along with accompanying clinical features, are widely recognized as indicative of crush syndrome. Diagnostic investigations commonly involve assessing serum levels of aldolase, myoglobin, and myoglobin degradation products. Progressive increases in serum levels of lactic acid, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) are observed, while levels of serum urea and creatinine exhibit a steep rise, particularly following prolonged compression, and serve as valuable predictors of renal failure. The treatment of crush syndrome requires a multidisciplinary approach that addresses the metabolic, cardiovascular, and renal complications associated with this condition. The mainstay of treatment includes early release of the affected limb or compartment, fluid resuscitation, correction of electrolyte abnormalities, and alkalinization of urine. Additionally, renal replacement therapy and hyperbaric oxygen therapy may be beneficial in managing acute kidney injury and tissue hypoxia, respectively. Crush syndrome, albeit infrequent, represents a potentially fatal medical condition that demands a thorough comprehension of its underlying pathophysiology, clinical manifestations, and treatment modalities. Early recognition and appropriate management of this condition can significantly r,educe morbidity and mortality associated with crush syndrome.

Proton nuclear magnetic resonance(~1H-NMR) is used to investigate the effect of Renshenjian Decoction on serum and urine metabolism of type 2 diabetic rats with insulin resistance induced by high-sugar and high-fat diet combined with low-dose streptozotocin(STZ). After the successful establishment of the insulin resistance model of type 2 diabetes, administration for 35 days, the serum and urine of rats were taken. Once the ~1H-NMR data have been collected and processed, PCA and OPLS-DA were used to analyze them. The results show that: compared with the blank group, the contents of methionine, taurine, α-glucose and β-glucose in the serum of the model group increased significantly(P&lt;0.001), while the contents of 3-hydroxybutyric acid, lactic acid and unsaturated fatty acids decreased significantly(P&lt;0.01). In the model group, the contents of trimethylamine oxide, glycine, α-glucose, β-glucose, taurine and phosphocholine in urine increased significantly(P&lt;0.05), while the contents of creatine, lactic acid, acetic acid and citric acid decreased significantly(P&lt;0.05). Compared with the model group, the contents of 3-hydroxybutyric acid and unsaturated fatty acids in serum of rats in the treatment group increased significantly(P&lt;0.05), while the contents of taurine, α-glucose and β-glucose decreased significantly(P&lt;0.01). In the treatment group, the contents of lactic acid, taurine and creatine in urine increased significantly(P&lt;0.05), while the contents of trimethylamine oxide, glycine, α-glucose, β-glucose and phosphocholine decreased significantly(P&lt;0.01). The results show that Renshenjian Decoction can regulate metabolic disorder and promote the metabolic phenotype to return to the normal range. It displayed therapeutic effect on type 2 diabetic rats with insulin resistance and provided a certain scientific basis for the biological basic research of Renshenjian Decoction by improving insulin resistance in diabetes mellitus.