Polysaccharides, predominantly extracted from traditional Chinese medicinal herbs such as Lycium barbarum, Angelica sinensis, Astragalus membranaceus, Dendrobium officinale, Ganoderma lucidum, and Poria cocos, represent principal bioactive constituents extensively utilized in Chinese medicine. These compounds have demonstrated significant anti-inflammatory capabilities, especially anti-liver injury activities, while exhibiting minimal adverse effects. This review summarized recent studies to elucidate the hepatoprotective efficacy and underlying molecular mechanisms of these herbal polysaccharides. It underscored the role of these polysaccharides in regulating hepatic function, enhancing immunological responses, and improving antioxidant capacities, thus contributing to the attenuation of hepatocyte apoptosis and liver protection. Analyses of molecular pathways in these studies revealed the intricate and indispensable functions of traditional Chinese herbal polysaccharides in liver injury management. Therefore, this review provides a thorough examination of the hepatoprotective attributes and molecular mechanisms of these medicinal polysaccharides, thereby offering valuable insights for the advancement of polysaccharide-based therapeutic research and their potential clinical applications in liver disease treatment.
Humans ; Drugs, Chinese Herbal/pharmacology* ; Liver Diseases/drug therapy* ; Antioxidants ; Polysaccharides/therapeutic use* ; Medicine, Chinese Traditional

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Objective:To investigate the prognostic value of N-terminal B-type brain natriuretic peptide precursor (NT-proBNP), cardiac troponin I (cTnI) and aVL lead T-wave changes in acute coronary syndrome (ACS).Methods:Clinical data of 162 patients with ACS admitted to the Emergency Chest Pain Center of the Affiliated Hospital of Jining Medical University from January 2020 to December 2021 were retrospectively collected, including 84 patients with unstable angina pectoris (UAP) and 46 patients with ST-segment elevation myocardial infarction (STEMI). 32 patients with non-ST elevation myocardial infarction (NSTEMI); There were 66 patients with single-vessel disease, 70 patients with double-vessel disease, 26 patients with multi-vessel disease, and 51 patients with major cardiovascular adverse events (MACE). The levels of NT-proBNP, cTnI and T-wave change ratio of aVL lead were compared in different patients.Results:The NT-proBNP and cTnI of UAP patients were 510.42(365.56, 630.54)pg/ml and 8.20(6.50, 10.50)ng/ml, respectively, which were significantly lower than those of STEMI and NSTEMI patients (all P<0.05). There was no significant difference in NT-proBNP and cTnI between STEMI and NSTEMI patients (all P>0.05). The T-wave change proportions of NT-proBNP, cTnI and aVL leads in patients with multi-vessel lesions were 804.90(680.87, 980.05)pg/ml, 13.90(10.12, 15.65)ng/ml and 88.46%(23/26), respectively. It was significantly higher than that in patients with single and double vessel lesions (all P<0.05). The T-wave change ratio of NT-proBNP, cTnI and aVL leads in patients with double-vessel disease was 680.84(525.50, 810.62)pg/ml, 10.40(8.92, 13.60)ng/ml and 67.14%(47/70), respectively, which was significantly higher than that in patients with single-vessel disease (all P<0.05). The proportions of T-wave changes of NT-proBNP, cTnI and aVL leads in MACE patients were 744.54(621.17, 905.54)pg/ml, 12.21(8.65, 15.54)ng/ml and 86.27%(44/51), respectively. It was significantly higher than those without MACE (all P<0.05). The area under receiver operating characteristic (ROC) curve of NT-proBNP, cTnI and aVL lead T-wave changes independently and jointly predicted the occurrence of MACE were 0.937, 0.677, 0.706 and 0.799, respectively, among which NT-proBNP had a higher value in predicting the occurrence of MACE. Conclusions:The T-wave changes of NT-proBNP, cTnI and aVL leads are related to the type of lesions, the number of lesions and the occurrence of MACE in ACS patients, and NT-proBNP has a high value in predicting prognosis.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Based on the resutls of literature review and interviews of experts, two rounds of Delphi surveys were conducted. The mean, importance ratio, coefficient of variation and coordination coefficient were used for assessment of survey from multiple perspectives, and finally form a framework model of factors affecting the efficacy of Tuina therapy. A total of 37 experts were selected for questionnaire surveys, the positive coefficients of experts' participatation in the first round and second round were 92.5% and 80.0%, respectively. The overall coordination coefficient in the second round is 0.68. The items were included into the consensus meeting if the importance ratio of items were equal to and more than 80%. After the expert consensus meeting, 22 items were included to form a framework model of factors affecting the efficacy of Tuina therapy, and summarized as 5 major influencing factors, including diagnostic factors, treatment factors, prognostic factors, patient factors, and doctor-patient communication. This framework can guide and help young Tuina practitioners to improve clinical efficacy. It is also clearly pointed out that the effect of Tuina for pain is not only related to disease diagnosis or manipulation, but also related to home exercise, health care, and doctor-patient communication.

Tuina (Chinese massage) is an important part of Traditional Chinese Medicine. It is a simple and inexpensive technique, and has shown effectiveness for muscle and bone diseases, visceral diseases, gynecological diseases, and common diseases in children. This paper aims to analyze the factors influencing the effects of Tuina. The factors included the aspects of diagnosis, treatment, prognosis, patient factors and doctor-patient communication. During the treatment of Tuina, doctors should carry out good doctor-patient communication, properly evaluate and exam patients, and clarify diagnosis, take appropriate Tuina techniques according to the patients' constitution, health condition, and comorbidity. Only in such way, could Tuina achieve effectiveness and safety.

Diabetic kidney disease (DKD) is the most common complication of diabetes mellitus (DM). Qianjin Wenwu decoction (QWD), a well-known traditional Korean medicine, has been used for the treatment of DKD, with satisfactory therapeutic effects. This study was designed to investigate the active components and mechanisms of action of QWD in the treatment of DKD. The results demonstrated that a total of 13 active components in five types were found in QWD, including flavonoids, flavonoid glycosides, phenylpropionic acids, saponins, coumarins, and lignins. Two key proteins, TGF-β1 and TIMP-1, were identified as the target proteins through molecular docking. Furthermore, QWD significantly suppressed Scr and BUN levels which increased after unilateral ureteral obstruction (UUO). Hematoxylin & eosin (H&E) and Masson staining results demonstrated that QWD significantly alleviated renal interstitial fibrosis in UUO mice. We also found that QWD promoted ECM degradation by regulating MMP-9/TIMP-1 homeostasis to improve renal tubulointerstitial fibrosis and interfere with the expression and activity of TGF- β1 in DKD treatment. These findings explain the underlying mechanism of QWD for the treatment of DKD, and also provide methodological reference for investigating the mechanism of traditional medicine in the treatment of DKD.
Rats ; Mice ; Animals ; Ureteral Obstruction/metabolism* ; Kidney/metabolism* ; Tissue Inhibitor of Metalloproteinase-1/metabolism* ; Molecular Docking Simulation ; Rats, Sprague-Dawley ; Kidney Diseases/drug therapy* ; Extracellular Matrix/metabolism* ; Flavonoids/metabolism* ; Fibrosis

Objective:An early diagnosis model of acute aortic dissection (AAD) was established based on chest pain center database.Methods:The clinical data of patients who attended Chest Pain Center of Department of Emergency in Affiliated Hospital of Jining Medical University of Shandong Province from January 2020 to December 2020 were retrospectively collected. Patients were divided into AAD and non-AAD groups according to whether or not AAD was diagnosed. The clinical related indicators of the two groups were compared. The research indicators with statistical differences between the two groups were included in multivariate Logistic regression analysis, and the early diagnosis of AAD nomogram model was established. The receiver operating characteristic (ROC) curve of the model was used to evaluate the prediction accuracy, and the Homser-Lemeshow statistics were used to test the goodness of fit for the model. A total of 630 patients with chest pain who visited the hospital from January 2021 to March 2021 were also collected for external validation of the model. The t-test of independent samples was used to compare the measurement data of normal distribution, nonparametric test was used to compare the measurement data of skewness distribution, and χ 2 test was used to compare the counting data between groups. Results:A total of 2 738 patients were included, of which 4.09% (112/2 738) were AAD patients. Univariate analysis showed that in AAD group, male morbidity (74.11%(83/112)), hypertension history (70.54%(79/112)), aortic disease history (10.71%(12/112)), family history of aortic disease (4.46%(5/112)), sudden onset of symptoms (76.79%(86/112)), percentage of patients with laceration pain (38.39%(43/112)), patients with back pain (66.07%(74/112)), patients with abdominal pain (16.96%(19/112)), systolic blood pressure ((159.44±30.94) mmHg), bilateral blood pressure/pulse asymmetry (23.21% (26/112)), incidence of complicated neurological signs (7.14%(8/112)) and D-dimer (3.57(2.10, 6.62) mg/L) were significantly higher than those in non-AAD group (59.56%(1 564/2 626), 46.23%(1 214/2 626), 0.23%(6/2 626), 0.08%(2/2 626), 35.99%(945/2 626), 0.08%(2/2 626), 3.08%(81/2 626), 3.81%(100/2 626), (142.46±27.90) mmHg, 0.15%(4/2 626), 0.27%(7/2 626), 0.31(0.20, 0.50) mg/L). Age ((57.95±14.35) years old) and CK-MB (1.50(0.90, 3.25) μg/L) were significantly lower than those in the non-AAD group ((61.94±15.77) years, 2.50(1.24, 4.81) μg/L). The differences were statistically significant (the statistical values were χ 2=9.47, χ 2=25.46, χ 2=180.80, χ 2=81.11, χ 2=76.17, χ 2=975.60, χ 2=798.00, χ 2=44.72, t=6.28, χ 2=527.20, χ 2=93.22, Z=14.09, t=2.61, and Z=3.51, respectively; P values were 0.002, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, 0.009, and <0.001, respectively). Multivariate analysis showed that history of hypertension ( OR=3.088, 95% CI:1.294-7.374), history of aortic disease ( OR=20.771, 95% CI:2.132-202.361), family history of aortic disease ( OR=266.425, 95% CI:17.610-4 030.851), sudden onset of symptoms ( OR=3.538, 95% CI:1.643-7.619), laceration pain ( OR=1 771.971, 95% CI:204.048-15 387.935), back pain ( OR=61.550,95% CI:27.987-135.367), abdominal pain ( OR=12.325, 95% CI:4.201-36.161), systolic blood pressure ( OR=1.026, 95% CI:1.013-1.039), bilateral blood pressure/pulse asymmetry ( OR=338.357, 95% CI:60.704-1 885.949) and D-dimer ( OR=1.241, 95% CI:1.176-1.309) were independent factors for the diagnosis of AAD in patients with chest pain (P values were 0.011, 0.009, <0.001, 0.001, <0.001, <0.001, <0.001, <0.001, <0.001, and <0.001, respectively). Furthermore, the nomogram model was constructed. ROC curve analysis showed that the area under the curve was 0.976 ( P<0.01), the specificity was 94.52%, and the sensitivity was 91.96%. The statistics of Homser-lemeshow was used to test the goodness of fit, which shows that the model can be fitted well (χ 2=2.928, P=0.939). The prediction model was verified by external validation data, and the area under the ROC curve was 0.934 ( P<0.01), indicating that the model had good prediction performance. Conclusions:History of hypertension, history of aortic disease, family history of aortic disease, sudden onset of symptoms, laceration pain, back pain, abdominal pain, systolic blood pressure, bilateral blood pressure/pulse asymmetry and D-dimer were independent factors for the diagnosis of AAD in patients with acute chest pain. The AAD early diagnosis nomogram model based on the above factors has good predictive performance.