Functional constipation （FC） is a common functional disorder of the intestines， mainly characterized by reduced bowel movement frequency， difficulty in defecation， a sensation of incomplete evacuation， and hard stools， which severely affect patients’ quality of life. Research indicates that the pathogenesis of FC is closely related to gut microbiota dysbiosis and abnormal bile acid secretion. Bile acids， as endogenous natural laxatives， promote bowel movements by enhancing colonic secretion and regulating intestinal motility； meanwhile， gut microbiota influence colonic transit function by regulating the enteric nervous system， immune system， and their metabolic products. Based on an overview of the relationship between gut microbiota and bile acid metabolism， this article systematically reviews the current research status on the mechanisms of traditional Chinese medicine （TCM） in treating FC by regulating the balance of the gut microbiota-bile acid axis. It is found that single Chinese medicinal herbs （such as Atractylodes macrocephala）， isolated compounds （such as Platycodon grandiflorum polysaccharides）， herbal formulas （such as Shanger huang pill）， acupuncture， and moxibustion can up-regulate the abundance of beneficial bacteria， reshape the microbial structure， correct bile acid metabolism， and activate the Takeda G-protein receptor 5/farnesoid X receptor pathway to treat FC.

ObjectiveTo study the chemical constituents of Bidens pilosa and the in vitro antiproliferative activity of some compounds against gastric cancer cells. MethodsThe chemical constituents were isolated and purified by methods such as silica gel column chromatography， preparative thin layer chromatography， medium pressure preparation chromatography， semi-preparative high performance liquid chromatography（HPLC） and recrystallization， their structures were identified on the basis of physicochemical properties， spectral data and circular dichroism spectra. Thiazole blue（MTT） assay was used to determine the in vitro inhibitory activityies of some isolated compounds against human gastric cancer SGC-7901 cells， and molecular docking was used to predict their potential targets. ResultsTwenty-five compounds were isolated from the petroleum ether fraction of B. pilosa and identified as bidpillignan A（1）， 5α， 8α-epidioxy-（22E， 24R）-ergosta-6， 22-diene-3β-ol（2）， 3β-hydroxysitost-5-en-7-one（3）， （20R）-6β-hydroxystigmasta-4， 22-dien-3-one（4）， 3β-hydroxylstigmasta-5， 22-dien-7-one（5）， （22E， 24S）-24-methyl-5α-choleata-7， 22-diene-3β， 5α， 6β-triol（6）， stigamast-5-ene-3β， 7α-diol（7）， stigmast-5， 22-diene-3β， 7α-diol（8）， 7β-hydroxysitosterol（9）， stigmasterol（10）， artabotrol（11）， cosmosoic acid（12）， ent-4（15）-eudesmene-1β， 6α-diol（13）， clovandiol（14）， 1H-indole-3-carboxaldehyde（15）， 6， 7-dimethoxycoumarin（16）， 3'， 4'-dimethoxyquercetin（17）， 8， 8'-bis-（dihydroconiferyl）-diferuloylate（18）， hydroxydihydrobovolide（19）， 2-deacetyl-11β， 13-dihydroxyxanthinin（20）， loliolide（21）， pubescone（22）， （+）-dehydrovomifoliol（23）， 2， 3-dihydroxypropyl palmitate（24） and n-hexadecane acid（25）. Among them， compound 1 was a new compound， compounds 3-9， 11-12， 18-20， 22-23 were first isolated from Bidens genus plants， and compounds 13 and 14 were isolated from this plant for the first time. Compounds 17 and 18 showed good in vitro proliferation inhibitory activities against SGC-7901 cells with the half inhibitory concentrations（IC₅₀） of 3.11， 7.22 μmol·L^-1， respectively. Molecular docking results showed that the potential targets of the two exerting anti-gastric cancer activity might be vascular endothelial growth factor receptor 2（VEGFR2） and poly（adenosine diphosphate-ribose） polymerase 7（PARP7）. ConclusionOne new compound， 14 genus first compounds， and 2 species first compounds were isolated from B. pilosa， among which compounds 17 and 18 processed anti-gastric cancer cell proliferation activity in vitro， and the targets may be VEGFR2 and PARP7.

Objective To investigate the cognition level and behavior compliance of blood pressure measurement in community residents and analyze the related influencing factors, and to provide evidence for community health management and blood pressure control. Methods A questionnaire survey was conducted to investigate 4470 community patients. Questionnaires included basic personal information，blood pressure measurement cognition, and blood pressure measurement behavior related issues. SPSS 19.0 was used to analyze the basic information, blood pressure measurement cognition, and pressure measurement behavior of the survey subjects. Logistic regression was performed to analyze relevant factors affecting blood pressure measurement cognition and behavior compliance. Results The overall cognitive compliance rate for blood pressure measurement among the visiting community patients was 31.52%. Age, education level, and chronic disease had a statistically significant impact on the cognitive knowledge (P<0.05). The overall behavior compliance rate of blood pressure measurement among the community patients was 23.69%. The cognition, age and education had a statistically significant impact on the overall behavior compliance rate of blood pressure measurement (P<0.05). Conclusion The cognitive level and standardized behavior of blood pressure measurement of community patients need to be improved. More attention should be paid to the elderly, low education level residents and community residents without chronic diseases, to promote community residents to form correct and standardized behavior of blood pressure measurement through health education.

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.

ObjectiveTo investigate the effects of different concentrations of Shaoyaotang-containing serum on lipopolysaccharide （LPS）-induced inflammation of human colorectal adenocarcinoma （Caco-2） cells by inhibiting apoptosis via activating the tumor necrosis factor （TNF） receptor superfamily member 6 （Fas）/Fas ligand （FasL） pathway. MethodsCaco-2 cells were allocated into blank， model （LPS， 10 mg·L^-1）， Shaoyaotang-containing serum （5%， 10%， 15%， 20%）， and Fas inhibitor （KR-33493， 20 mmol·L^-1） groups. Except the blank group， the other groups were stimulated with 10 mg·L^-1 LPS for 24 h for the modeling of inflammation. After successful modeling， the blank， Fas inhibitor， and model groups were treated with blank serum， and the Shaoyaotang-containing serum groups were treated with the serum samples at corresponding concentrations for 24 h. The Fas inhibitor group was subjected to KR-33493 pretreatment for 1 h. Cell proliferation and viability were examined by the cell-counting kit-8 （CCK-8） method. The levels of interleukin （IL）-6， IL-1β， and TNF-α were measured by enzyme-linked immunosorbent assay. Apoptosis was detected by flow cytometry. The protein and mRNA levels of Fas， FasL， cysteinyl aspartate-specific proteinase （Caspase）-3， Caspase-9， B-cell lymphoma 2 （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsCompared with the blank group， the model group presented a decrease in cell survival rate （P<0.01）. Compared with that in the model group， the cell survival rate showed no significant change in the 5% Shaoyaotang-containing serum group but increased in the 10%， 15%， and 20% Shaoyaotang-containing serum groups （P<0.01）. Since there was no statistical difference between the 5% Shaoyaotang-containing serum group and the model group， 10%， 15%， and 20% Shaoyaotang-containing sera were selected for the follow-up study. Compared with the blank group， the model group showed risen levels of IL-6， IL-1β， and TNF-α （P<0.01）， an increased apoptosis rate （P<0.01）， up-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.01）， and down-regulated protein and mRNA levels of Bcl-2 （P<0.01）. Compared with the model group， the Fas inhibitor group and the 10%， 15%， and 20% Shaoyaotang-containing serum groups showed declined levels of IL-6， IL-1β， and TNF-α （P<0.01）， decreased apoptosis rates （P<0.01）， down-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and up-regulated protein and mRNA levels of Bcl-2 （P<0.05， P<0.01）. In addition， the 15% and 20% Shaoyaotang-containing serum groups had lower levels of IL-6， IL-1β， and TNF-α （P<0.05， P<0.01）， lower apoptosis rates （P<0.05， P<0.01）， lower protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and higher protein and mRNA levels of Bcl-2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can reduce the content of inflammatory factors in Caco-2 cells， down-regulate the protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax， and up-regulate the protein and mRNA levels of Bcl-2 under the intervention of LPS by regulating the Fas/FasL pathway and inhibiting the apoptosis of intestinal epithelial cells in ulcerative colitis.

ObjectiveTo investigate the protective effect and mechanism of Shaoyaotang （SYD） on the lipopolysaccharide （LPS）-induced damage of tight junction proteins in the human colorectal adenocarcinoma （Caco-2） cell model of inflammation via the Ras homolog gene family member A （RhoA）/Rho-associated coiled-coil forming protein kinase （ROCK） pathway. MethodsCaco-2 cells were grouped as follows： Blank， model （LPS， 10 mg·L^-1）， SYD-containing serum （10%， 15%， and 20%）， and inhibitor （Fasudil， 25 μmol·L^-1）. After 24 hours of intervention， the cell viability in each group was examined by the cell-counting kit 8 （CCK-8） method. Enzyme-linked immunosorbent assay was employed to determine the levels of endothelin-1 （ET-1）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were employed to determine the mRNA and protein levels， respectively， of RhoA， ROCK2， claudin-5， and zonula occludens-1 （ZO-1） in cells of each group. ResultsCompared with the blank group， the model group showcased a marked reduction in the cell viability （P<0.01）， elevations in the levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， declines in both mRNA and protein levels of ZO-1 and claudin-5 （P<0.01）， and rises in mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Compared with the model group， the Shaoyaotang-containing serum （10%， 15%， and 20%） groups had enhanced cell viability （P<0.01）， lowered levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， up-regulated mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and down-regulated mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Moreover， the inhibitor group and the 15% and 20% Shaoyaotang-containing serum groups had lower levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.05， P<0.01）， higher mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and lower mRNA and protein levels of RhoA and ROCK2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can lower the levels of LPS-induced increases in levels of inflammatory cytokines and endothelin to ameliorate the damage of tight junction proteins of the Caco-2 cell model of inflammation by regulating the expression of proteins in the RhoA/ROCK pathway.

ObjectiveTo investigate the effects of different concentrations of Shaoyaotang-containing serum on lipopolysaccharide （LPS）-induced inflammation of human colorectal adenocarcinoma （Caco-2） cells by inhibiting apoptosis via activating the tumor necrosis factor （TNF） receptor superfamily member 6 （Fas）/Fas ligand （FasL） pathway. MethodsCaco-2 cells were allocated into blank， model （LPS， 10 mg·L^-1）， Shaoyaotang-containing serum （5%， 10%， 15%， 20%）， and Fas inhibitor （KR-33493， 20 mmol·L^-1） groups. Except the blank group， the other groups were stimulated with 10 mg·L^-1 LPS for 24 h for the modeling of inflammation. After successful modeling， the blank， Fas inhibitor， and model groups were treated with blank serum， and the Shaoyaotang-containing serum groups were treated with the serum samples at corresponding concentrations for 24 h. The Fas inhibitor group was subjected to KR-33493 pretreatment for 1 h. Cell proliferation and viability were examined by the cell-counting kit-8 （CCK-8） method. The levels of interleukin （IL）-6， IL-1β， and TNF-α were measured by enzyme-linked immunosorbent assay. Apoptosis was detected by flow cytometry. The protein and mRNA levels of Fas， FasL， cysteinyl aspartate-specific proteinase （Caspase）-3， Caspase-9， B-cell lymphoma 2 （Bcl-2）， and Bcl-2-associated X protein （Bax） were determined by Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. ResultsCompared with the blank group， the model group presented a decrease in cell survival rate （P<0.01）. Compared with that in the model group， the cell survival rate showed no significant change in the 5% Shaoyaotang-containing serum group but increased in the 10%， 15%， and 20% Shaoyaotang-containing serum groups （P<0.01）. Since there was no statistical difference between the 5% Shaoyaotang-containing serum group and the model group， 10%， 15%， and 20% Shaoyaotang-containing sera were selected for the follow-up study. Compared with the blank group， the model group showed risen levels of IL-6， IL-1β， and TNF-α （P<0.01）， an increased apoptosis rate （P<0.01）， up-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.01）， and down-regulated protein and mRNA levels of Bcl-2 （P<0.01）. Compared with the model group， the Fas inhibitor group and the 10%， 15%， and 20% Shaoyaotang-containing serum groups showed declined levels of IL-6， IL-1β， and TNF-α （P<0.01）， decreased apoptosis rates （P<0.01）， down-regulated protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and up-regulated protein and mRNA levels of Bcl-2 （P<0.05， P<0.01）. In addition， the 15% and 20% Shaoyaotang-containing serum groups had lower levels of IL-6， IL-1β， and TNF-α （P<0.05， P<0.01）， lower apoptosis rates （P<0.05， P<0.01）， lower protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax （P<0.05， P<0.01）， and higher protein and mRNA levels of Bcl-2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can reduce the content of inflammatory factors in Caco-2 cells， down-regulate the protein and mRNA levels of Fas， FasL， Caspase-3， Caspase-9， and Bax， and up-regulate the protein and mRNA levels of Bcl-2 under the intervention of LPS by regulating the Fas/FasL pathway and inhibiting the apoptosis of intestinal epithelial cells in ulcerative colitis.

ObjectiveTo investigate the protective effect and mechanism of Shaoyaotang （SYD） on the lipopolysaccharide （LPS）-induced damage of tight junction proteins in the human colorectal adenocarcinoma （Caco-2） cell model of inflammation via the Ras homolog gene family member A （RhoA）/Rho-associated coiled-coil forming protein kinase （ROCK） pathway. MethodsCaco-2 cells were grouped as follows： Blank， model （LPS， 10 mg·L^-1）， SYD-containing serum （10%， 15%， and 20%）， and inhibitor （Fasudil， 25 μmol·L^-1）. After 24 hours of intervention， the cell viability in each group was examined by the cell-counting kit 8 （CCK-8） method. Enzyme-linked immunosorbent assay was employed to determine the levels of endothelin-1 （ET-1）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were employed to determine the mRNA and protein levels， respectively， of RhoA， ROCK2， claudin-5， and zonula occludens-1 （ZO-1） in cells of each group. ResultsCompared with the blank group， the model group showcased a marked reduction in the cell viability （P<0.01）， elevations in the levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， declines in both mRNA and protein levels of ZO-1 and claudin-5 （P<0.01）， and rises in mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Compared with the model group， the Shaoyaotang-containing serum （10%， 15%， and 20%） groups had enhanced cell viability （P<0.01）， lowered levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.01）， up-regulated mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and down-regulated mRNA and protein levels of RhoA and ROCK2 （P<0.01）. Moreover， the inhibitor group and the 15% and 20% Shaoyaotang-containing serum groups had lower levels of ET-1， TNF-α， IL-1β， and IL-6 （P<0.05， P<0.01）， higher mRNA and protein levels of ZO-1 and claudin-5 （P<0.05， P<0.01）， and lower mRNA and protein levels of RhoA and ROCK2 （P<0.05， P<0.01） than the 10% Shaoyaotang-containing serum group. ConclusionThe Shaoyaotang-containing serum can lower the levels of LPS-induced increases in levels of inflammatory cytokines and endothelin to ameliorate the damage of tight junction proteins of the Caco-2 cell model of inflammation by regulating the expression of proteins in the RhoA/ROCK pathway.

Objective: The CT/MRI Liver Imaging Reporting and Data System (LI-RADS) demonstrates high specificity with relatively limited sensitivity for diagnosing hepatocellular carcinoma (HCC) in high-risk patients. This study aimed to explore the possibility of improving sensitivity by combining CT/MRI LI-RADS v2018 with second-line contrast-enhanced ultrasound (CEUS) LI-RADS v2017 using sulfur hexafluoride (SHF) or perfluorobutane (PFB). Materials and Methods: This retrospective analysis of prospectively collected multicenter data included high-risk patients with treatment-naive hepatic observations. The reference standard was pathological confirmation or a composite reference standard (only for benign lesions). Each participant underwent concurrent CT/MRI, SHF-enhanced US, and PFB-enhanced US examinations. The diagnostic performances for HCC of CT/MRI LI-RADS alone and three combination strategies (combining CT/ MRI LI-RADS with either LI-RADS SHF, LI-RADS PFB, or a modified algorithm incorporating the Kupffer-phase findings for PFB [modified PFB]) were evaluated. For the three combination strategies, apart from the CT/MRI LR-5 criteria, HCC was diagnosed if CT/MRI LR-3 or LR-4 observations met the LR-5 criteria using LI-RADS SHF, LI-RADS PFB, or modified PFB. Results: In total, 281 participants (237 males; mean age, 55 ± 11 years) with 306 observations (227 HCCs, 40 non-HCC malignancies, and 39 benign lesions) were included. Using LI-RADS SHF, LI-RADS PFB, and modified PFB, 20, 23, and 31 CT/MRI LR-3/4 observations, respectively, were reclassified as LR-5, and all were pathologically confirmed as HCCs. Compared to CT/MRI LI-RADS alone (74%, 95% confidence interval [CI]: 68%–79%), the three combination strategies combining CT/MRI LI-RADS with either LI-RADS SHF, LI-RADS PFB, or modified PFB increased sensitivity (83% [95% CI: 77%–87%], 84% [95% CI: 79%–89%], 88% [95% CI: 83%–92%], respectively; all P < 0.001), while maintaining the specificity at 92% (95% CI: 84%–97%). Conclusion The combination of CT/MRI LI-RADS with second-line CEUS using SHF or PFB improved the sensitivity of HCC diagnosis without compromising specificity.