In recent years， as the incidence of ulcerative colitis （UC） is growing， intestinal mucosal injury has garnered increasing attention， and it is characterized by high recurrence， risk of inflammation-cancer transformation， and difficulty in repair. Intestinal mucosal injury in UC is centered on persistent inflammation and barrier dysfunction， with its pathological mechanisms involving endoplasmic reticulum stress （ERS）-mediated changes such as abnormal apoptosis， abnormal autophagy， and inflammatory responses. ERS induces apoptosis of intestinal epithelial cells， disrupts tight junction proteins， and exacerbates inflammatory responses through pathways such as protein kinase R-like endoplasmic reticulum kinase （PERK）， inositol-requiring enzyme 1 alpha （IRE1α）， and activating transcription factor 6 （ATF6）， ultimately causing intestinal mucosal injury. Traditional Chinese medicine （TCM） has a long history of research on UC. The theory of sores depending on spleen-earth holds that spleen deficiency is the fundamental cause of UC， while pathological products such as dampness-turbidity and blood stasis are the secondary manifestations. Dysfunction of the spleen-earth leads to insufficient production and transformation of Qi and blood， malnutrition of the intestinal mucosa， and invasion of external pathogens. In the active phase of UC， spleen deficiency is often accompanied by excessive pathogenic factors such as dampness-heat and heat-toxin， leading to acute intestinal mucosal damage. In the remission phase， however， it is mainly characterized by spleen deficiency and healthy Qi deficiency， accompanied by residual pathogens， resulting in weak intestinal mucosal repair. Studies have shown that the endoplasmic reticulum， as a key site for protein synthesis and folding， has functions highly similar to the TCM concept of the spleen governing transportation and transformation. From a TCM perspective， the endoplasmic reticulum can be regarded as the carrier of spleen transportation， and ERS is a microcosmic manifestation of spleen dysfunction， leading to intestinal mucosal injury. ERS impairs the structure and function of the endoplasmic reticulum， induces the generation of abnormal Qi， and triggers pathological changes， making inflammation difficult to be reduced and causing the aggravation of ERS， forming a vicious cycle of spleen deficiency-pathological products-intestinal injury. TCM has unique advantages in regulating ERS to prevent and treat intestinal mucosal injury. According to the theory of sores depending on spleen-earth and the modern medical understanding of ERS， this paper delves into the TCM and Western medicine pathogenesis of intestinal mucosal injury in UC. Furthermore， this paper discusses the roles of TCM active components and compound formulas in reducing intestinal mucosal injury in UC by regulating ERS under the guidance of the treatment principles of invigorating the spleen and replenishing Qi as the key and dispelling dampness and removing blood stasis as the supplementation， aiming to provide new ideas and methods for the prevention and treatment of UC.

ObjectiveTo investigate the role of silent information regulatory protein （SIRT6）/hypoxia-inducible factor-1α （HIF-1α） pathway in regulating the reprogramming of glucose metabolism in ulcerative colitis （UC） and the mechanism of intervention of Shaoyaotang. MethodsForty-eight c57bL/6 mice were randomly divided into a blank group， a model group， a Mesalazine group （0.42 g·kg^-1）， a Shaoyaotang group （31.08 g·kg^-1）， an inhibitor group （OSS-128167， 50 mg·kg^-1）， and an inhibitor + Shaoyaotang group （50 mg·kg^-1 OSS-128167 + 31.08 g·kg^-1 Shaoyaotang）. A UC model was established by the administration of 2.5% dextran sulfate sodium （DSS） solution for mice in other groups for 7 d， except for the blank group. The mice in each group were treated with saline， Mesalazine， Shaoyaotang， inhibitor， and inhibitor + Shaoyaotang， respectively， for 7 d. The mice were necropsied 24 h after the last administration of the drug. The blood was collected from the orbital region， and colon tissue was taken. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in colon tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to detect serum interleukin （IL）-10， IL-17， and IL-6 levels. A biochemical method was used to detect glucose and lactate dehydrogenase A （LDHA） levels. Immunohistochemistry （IHC） was employed to detect IL-22 and transforming growth factor-β₁ （TGF-β₁） levels in colon tissue， and Western blot and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect relative protein and mRNA expressions of SIRT6， HIF-1α， and LDHA. ResultsCompared with those of the blank group， disease activity index （DAI） scores of mice in the model group and inhibitor group were significantly increased （P<0.01）. The length of colon tissue was significantly shortened， and colon tissue was congested and eroded. The pathohistological scores were significantly increased （P<0.01）. The levels of serum inflammatory factors IL-17 and IL-6 were significantly elevated， and the levels of IL-10 were significantly decreased （P<0.01）. The protein expressions of IL-22 and TGF-β₁ were significantly reduced in colon tissue （P<0.01）. The relative protein and mRNA expressions of SIRT6 were significantly decreased （P<0.01）， and the relative protein and mRNA expressions of HIF-1α and LDHA and the contents of glucose and lactate were significantly elevated （P<0.01）. The level of inflammation in the colon of the mice in the inhibitor group was more severe than that in the model group （P<0.01）. Compared with the model group， the Mesalazine group， the Shaoyaotang group， and the inhibitor + Shaoyaotang group showed reduced colonic injury， significant decrease in serum IL-17 and IL-6， significant increase in IL-10 （P<0.01）， significant increase in the protein expressions of IL-22 and TGF-β₁ in colon tissue （P<0.01）， significant increase in the protein expressions of SIRT6 and the relative mRNA expressions （P<0.01）， and significant reduction in the protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate （P<0.01）. Compared with those in the Shaoyaotang group， the serum IL-17 and IL-6 were significantly increased， and IL-10 was significantly decreased in the inhibitor + Shaoyaotang group （P<0.01）. The protein expressions of IL-22 and TGF-β₁ in colon tissue were significantly decreased （P<0.01）. The expressions of SIRT6 protein and the relative mRNA expressions were significantly decreased （P<0.01）. The protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate were significantly elevated （P<0.01）. However， the difference between the Shaoyaotang group and the Mesalazine group was not significant. ConclusionShaoyaotang can effectively treat DSS-induced mice with UC through the SIRT6/HIF-1α pathway， and its mechanism of action may be related to the regulation of the SIRT6/HIF-1α pathway and glucose metabolism reprogramming and the inhibition of glycolysis.

ObjectiveTo investigate the role of silent information regulatory protein （SIRT6）/hypoxia-inducible factor-1α （HIF-1α） pathway in regulating the reprogramming of glucose metabolism in ulcerative colitis （UC） and the mechanism of intervention of Shaoyaotang. MethodsForty-eight c57bL/6 mice were randomly divided into a blank group， a model group， a Mesalazine group （0.42 g·kg^-1）， a Shaoyaotang group （31.08 g·kg^-1）， an inhibitor group （OSS-128167， 50 mg·kg^-1）， and an inhibitor + Shaoyaotang group （50 mg·kg^-1 OSS-128167 + 31.08 g·kg^-1 Shaoyaotang）. A UC model was established by the administration of 2.5% dextran sulfate sodium （DSS） solution for mice in other groups for 7 d， except for the blank group. The mice in each group were treated with saline， Mesalazine， Shaoyaotang， inhibitor， and inhibitor + Shaoyaotang， respectively， for 7 d. The mice were necropsied 24 h after the last administration of the drug. The blood was collected from the orbital region， and colon tissue was taken. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in colon tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to detect serum interleukin （IL）-10， IL-17， and IL-6 levels. A biochemical method was used to detect glucose and lactate dehydrogenase A （LDHA） levels. Immunohistochemistry （IHC） was employed to detect IL-22 and transforming growth factor-β₁ （TGF-β₁） levels in colon tissue， and Western blot and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect relative protein and mRNA expressions of SIRT6， HIF-1α， and LDHA. ResultsCompared with those of the blank group， disease activity index （DAI） scores of mice in the model group and inhibitor group were significantly increased （P<0.01）. The length of colon tissue was significantly shortened， and colon tissue was congested and eroded. The pathohistological scores were significantly increased （P<0.01）. The levels of serum inflammatory factors IL-17 and IL-6 were significantly elevated， and the levels of IL-10 were significantly decreased （P<0.01）. The protein expressions of IL-22 and TGF-β₁ were significantly reduced in colon tissue （P<0.01）. The relative protein and mRNA expressions of SIRT6 were significantly decreased （P<0.01）， and the relative protein and mRNA expressions of HIF-1α and LDHA and the contents of glucose and lactate were significantly elevated （P<0.01）. The level of inflammation in the colon of the mice in the inhibitor group was more severe than that in the model group （P<0.01）. Compared with the model group， the Mesalazine group， the Shaoyaotang group， and the inhibitor + Shaoyaotang group showed reduced colonic injury， significant decrease in serum IL-17 and IL-6， significant increase in IL-10 （P<0.01）， significant increase in the protein expressions of IL-22 and TGF-β₁ in colon tissue （P<0.01）， significant increase in the protein expressions of SIRT6 and the relative mRNA expressions （P<0.01）， and significant reduction in the protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate （P<0.01）. Compared with those in the Shaoyaotang group， the serum IL-17 and IL-6 were significantly increased， and IL-10 was significantly decreased in the inhibitor + Shaoyaotang group （P<0.01）. The protein expressions of IL-22 and TGF-β₁ in colon tissue were significantly decreased （P<0.01）. The expressions of SIRT6 protein and the relative mRNA expressions were significantly decreased （P<0.01）. The protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate were significantly elevated （P<0.01）. However， the difference between the Shaoyaotang group and the Mesalazine group was not significant. ConclusionShaoyaotang can effectively treat DSS-induced mice with UC through the SIRT6/HIF-1α pathway， and its mechanism of action may be related to the regulation of the SIRT6/HIF-1α pathway and glucose metabolism reprogramming and the inhibition of glycolysis.

Objective To evaluate the prognostic value of microsatellite instability(MSI),preoperative D-dimer(DD),and CA19-9 level for the prognosis of colorectal cancer(CRC)patients who had undergone radical resection.Methods Retrospectively analyzed the general clinical data,MSI,DD,and CA19-9 levels of 81 CRC patients who underwent radical resection in the First Affiliated Hospital of Guangxi Medical University and Guilin People's Hospital between January 2020 and December 2021.Screen and evaluate prognostic factors.Results There was a statistically significant difference in the incidence of MSI,preoperative DD,and CA19-9 expression levels between recurrence group and non recurrence group(P＜0.05).There was a statistically significant difference in the incidence of MSI,preoperative DD,and CA19-9 expression levels between death group and survival group(P＜0.05).Univariate and multivariate analyses MSI was identified as a protective factor against recurrence(P=0.018),and high levels of preoperative DD and CA1 9-9 were identified as independent risk factors for recurrence(P=0.020,P=0.042).MSI was identified as a protective factor against mortality in CRC patients(P=0.036),and high levels of preoperative DD and CA19-9 were identified as independent risk factors for mortality in CRC patients(P=0.010,P=0.017).The receiver operating characteristic curve showed that the area under the curve(AUC)of MSI,DD,and CA19-9 for predicting recurrence after CRC surgery were 0.643,0.599,and 0.644 respectively,for mortality,they were 0.646,0.642,and 0.693 respectively.The combined model for predicting recurrence and mortality yielded AUC were 0.776 and 0.825,respectively.Conclusion MSI is a protective factor for prognosis in CRC patients,whereas high levels of preoperative DD and CA19-9 are risk factors for poor prognosis.The combined detection of these three factors can optimize the risk stratification of CRC.

Objective To evaluate the prognostic value of microsatellite instability(MSI),preoperative D-dimer(DD),and CA19-9 level for the prognosis of colorectal cancer(CRC)patients who had undergone radical resection.Methods Retrospectively analyzed the general clinical data,MSI,DD,and CA19-9 levels of 81 CRC patients who underwent radical resection in the First Affiliated Hospital of Guangxi Medical University and Guilin People's Hospital between January 2020 and December 2021.Screen and evaluate prognostic factors.Results There was a statistically significant difference in the incidence of MSI,preoperative DD,and CA19-9 expression levels between recurrence group and non recurrence group(P＜0.05).There was a statistically significant difference in the incidence of MSI,preoperative DD,and CA19-9 expression levels between death group and survival group(P＜0.05).Univariate and multivariate analyses MSI was identified as a protective factor against recurrence(P=0.018),and high levels of preoperative DD and CA1 9-9 were identified as independent risk factors for recurrence(P=0.020,P=0.042).MSI was identified as a protective factor against mortality in CRC patients(P=0.036),and high levels of preoperative DD and CA19-9 were identified as independent risk factors for mortality in CRC patients(P=0.010,P=0.017).The receiver operating characteristic curve showed that the area under the curve(AUC)of MSI,DD,and CA19-9 for predicting recurrence after CRC surgery were 0.643,0.599,and 0.644 respectively,for mortality,they were 0.646,0.642,and 0.693 respectively.The combined model for predicting recurrence and mortality yielded AUC were 0.776 and 0.825,respectively.Conclusion MSI is a protective factor for prognosis in CRC patients,whereas high levels of preoperative DD and CA19-9 are risk factors for poor prognosis.The combined detection of these three factors can optimize the risk stratification of CRC.

Objective To investigate the efficacy and safety of early goal-directed sedation with dexme-detomidine in patients with septic shock.Methods This study is selected from August 2015 to December 2016 in our department 70 patients receiving treatment of septic shock,and through random sample table method divided into the control group and the study group two,there were 32 cases in control group,the control group selected ob-ject according to the conventional sedation treatment,namely the application of midazolam extraction treatment, the study group of 38 patients with septic shock in patients with application of dexmedetomidine sedation,analysis and application of different sedation method analysis of two groups of patients with septic shock. The efficacy and safety of observation and etc. Results Two groups of patients with different treatment methods,The onset time of the study group of patients with septic shock after sedation,h recovery time and time of mechanical ventilation was obviously better than the control group,the effect of difference(P < 0.05),has significant research value. Conclusions For patients with septic shock early goal orientation selection and application of sedation of dexme-detomidine can play a better effect,the more safe and effective,sedation score is high,it is worth of application in clinical treatment.

Objective To explore the clinical effect of acupuncture on acute renal injury of sepsis.Methods From January 2015 to May 2017,adult patients with sepsis who received ≥ 7 days of treatment were collected from the Central Hospital of Zhuzhou.The participants were randomly divided into the control group (n =35) and the treatment group (n =37),and the control group was given routine treatment according to the sepsis guidelines.On the basis of control group,the treatment group was given acupuncture treatment,acupoints Shenshu and Sanyinjiao,Taixi,Zusanli.The clinical effects of the two groups of patients were compared.Results The levels of cystatin C,blood urea nitrogen and creatinine in the treatment group were significantly lower than those in the control group (P ＜ 0.05).There was no significant difference in the number and proportion of patients with blood purification between the two groups (P ＞ 0.05),while the frequency and time of blood purification treatment in the treatment group were significantly lower than those in the control group (P ＜ 0.05).The levels of blood interleukin-6 and tumor necrosis factor-alpha in the treatment group were significantly lower than those in the control group (P ＜ 0.05).From the fourth day of treatment,the Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score in the treatment group was significantly lower than that in the control group (P ＜ 0.05).There was no significant difference in mortality between the two groups at 28 days (P ＞ 0.05).Conclusions Acupuncture of Shenshu,Sanyinjiao,Taixi,Zusanli can improve sepsis patients with acute kidney injury in renal function.