This study aims to investigate the protective effect of resveratrol against liver injury in hindlimb unloading rats. Thirty 2-month-old male SD rats were randomly divided into normal group (Control), hindlimb unloading model group (Model), and hindlimb unloading+resveratrol administration group (Model+Res). The Model + Res group was injected intraperitoneally with 30 mg/kg of resveratrol, and the Control and Model groups were injected intraperitoneally with an equal volume of 0.9% NaCl. Liver tissues were collected after 28 days and analyzed for oxidative stress, inflammatory factors, energy metabolism indices, Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity, and morphological changes were observed by hematoxylin-eosin staining. The protein expression levels of Bax, Bcl-2, p-PI3K, PI3K, p-AKT, and AKT were detected by Western blotting. Compared with the Control group, hepatocytes in the Model group showed swelling, abnormal morphology, nuclear consolidation, and cell membrane disruption. Oxidative stress, inflammatory factor levels, hepatic glycogen accumulation, and energy metabolism were increased in the liver tissues of the Model group, while resveratrol treatment significantly reversed these changes. The results of Western blotting showed that resveratrol significantly reduced the expression of Bax and increased the expression levels of Bcl-2, and the proteins of p-PI3K/PI3K and p-AKT/AKT expression levels. It is suggested that 28 days of hindlimb unloading treatment could lead to liver tissue injury in rats, which is manifested as oxidative stress, inflammatory response, energy metabolism disorder and increased apoptosis level, and resveratrol has a certain mitigating effect on this.
【Abstract】ObjectiveTo explore the mechanisms of anabolism intensified by recombination human growth hormone (GH) on the basis of total parenteral nutrition (TPN) during postoperative in gastrointestinal carcinoma patients. MethodsNinety-four gastrointestinal carcinoma patients undergone operation were randomly divided into TPN group and TPN+GH group. The levels of TNF-α, IL-1, IL-6 and CRP were detected in the first, third, seventh postoperative day. ResultsThe levels of TNF-α, IL-1, IL-6 and CRP were significantly lower in TPN+GH group than those in the TPN group at the first, third, seventh postoperative day （P＜0.01）. The levels of TNF-α, IL-1, IL-6 and CRP were significantly higher at the indicated time of postoperative days than the pre-operative days in the two groups (P＜0.01）. ConclusionBy inhibiting TNF-α, IL-1, IL-6 and CRP production in gastrointestinal carcinoma patients undergone operation and blocking high catabolism induced by inflammatory cytokines, GH promotes the synthesis of anabolism.
ObjectiveTo systematically review the effect of compound Danshen dripping pills combined with Western medicine on inflammatory factors and cardiac function after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction.MethodsDatabases including CNKI, WanFang Data, VIP, CBM, PubMed, Web of Science, EMbase and The Cochrane Library were searched for randomized controlled trials of compound Danshen dripping pills combined with Western medicine in the treatment of acute myocardial infarction after PCI. The retrieval time was from the establishment of the databases to June 11th, 2020. Two reviewers independently screened literature, extracted data and evaluated the risk bias of included studies. RevMan 5.3 software was used for meta-analysis.ResultsA total of 16 studies were included, involving 2 069 patients. The results of the meta-analysis showed that the combination of compound Danshen dripping pills could increase the left ventricular ejection fraction (MD =−4.74, 95%CI 4.07 to 5.42, P<0.01), decrease the B-type natriuretic peptide (SMD=−3.81, 95%CI −5.06 to −2.57, P<0.01), the level of interleukin-6 (SMD=−3.20, 95%CI −4.54 to −1.86, P<0.01) and level of tumor necrosis factor-a (SMD=−4.96, 95%CI −7.03 to −2.89, P<0.01).ConclusionsCurrent evidence suggests that the combination of compound Danshen dropping pills has potential benefits in inhibiting inflammation and improving cardiac function after PCI. Due to the limited quality and quantity of the included studies, more high-quality studies are required to verify the above conclusions.
ObjectiveTo investigate the effects of melatonin (MT) on bone mass and serum inflammatory factors in rats received ovariectomy (OVX) and to investigate the effects of MT on the levels of inflammatory factors in culture medium and osteogenic ability of bone marrow mesenchymal stem cells (BMSCs) stimulated by lipopolysaccharide. Methods Fifteen 12-week-old Sprague Dawley (SD) rats were randomly divided into 3 groups. The rats in Sham group only received bilateral lateral abdominal incision and suture, the rats in OVX group received bilateral OVX, and the rats in OVX+MT group received 100 mg/(kg·d) MT oral intervention after bilateral OVX. After 8 weeks, the levels of serum inflammatory factors [interleukin-1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α)] were detected using ELISA assay. Besides, the distal femurs were detected by Micro-CT to observe changes in bone mass and microstructure, and quantitatively measured bone volume fraction, trabecular thickness, and trabecular number. The BMSCs were extracted from the femurs of three 3-week-old SD rats using whole bone marrow culture method and passaged. The 3rd-5th passage BMSCs were cultured with different concentrations of MT (0, 1, 10, 100, 1 000 µmol/L), and the cell viability was then detected using cell counting kit 8 (CCK-8) to select the optimal concentration of MT for subsequent experiments. Cells were devided into osteogenic induction group (group A) and osteogenic induction+1/5/10 μg/mL lipopolysaccharide group (group B-D). The levels of inflammatory factors (IL-1β, IL-6 and TNF-α) in cell culture medium were detected using ELISA assay after corresponding intervention. According to the results of CCK-8 method and ELISA detection, the cells were intervened with the most significant concentration of lipopolysaccharide for stimulating inflammation and the optimal concentration of MT with osteogenic induction, defining as group E, and the cell culture medium was collected to detect the levels of inflammatory factors by ELISA assay. After that, alkaline phosphatase (ALP) staining and alizarin red staining were performed respectively in groups A, D, and E, and the expression levels of osteogenic related genes [collagen type Ⅰ alpha 1 chain (Col1a1) and RUNX family transcription factor 2 (Runx2)] were also detected by real time fluorescence quantitative PCR (RT-qPCR). ResultsELISA and Micro-CT assays showed that compared with Sham group, the bone mass of the rats in the OVX group significantly decreased, and the expression levels of serum inflammatory factors (IL-1β, IL-6, and TNF-α) in OVX group significantly increased (P<0.05). Significantly, the above indicators in OVX+MT group were all improved (P<0.05). Rat BMSCs were successfully extracted, and CCK-8 assay showed that 100 µmol/L was the maximum concentration of MT that did not cause a decrease in cell viability, and it was used in subsequent experiments. ELISA assays showed that compared with group A, the expression levels of inflammatory factors (IL-1β, IL-6, and TNF-α) in the cell culture medium of groups B-D were significantly increased after lipopolysaccharide stimulation (P<0.05), and in a concentration-dependent manner. Moreover, the expression levels of inflammatory factors in group D were significantly higher than those in groups B and C (P<0.05). After MT intervention, the expression levels of inflammatory factors in group E were significantly lower than those in group D (P<0.05). ALP staining, alizarin red staining, and RT-qPCR assays showed that compared with group A, the percentage of positive area of ALP and alizarin red and the relative mRNA expressions of Col1a1 and Runx2 in group D significantly decreased, while the above indicators in group E significantly improved after MT intervention (P<0.05). ConclusionMT may affect the bone mass of postmenopausal osteoporosis by reducing inflammation in rats; MT can reduce the inflammation of BMSCs stimulated by lipopolysaccharide and weaken its inhibition of osteogenic differentiation of BMSCs.
ObjectiveTo investigate whether the miR-33s negatively regulates LPS-induced production of inflammatory cytokines by targeting p38 MAPK. MethodsHuman monocytes THP-1 cells were cultured in vitro and transfected with miR-33s mimic (25 nmol/L) or miR-33s inhibitor (25 nmol/L)by TransIT-X2® Dynamic Delivery System for 24 h. Then the transfected THP-1 cells were stimulated by LPS of 10.0 ng/mL for 24 h. The expression of miR-33s and p38 MAPK protein were measured by semi-quantitative RT-PCR. The concentrations of TNF-α,IL-6 and IL-1β in the cultured supernatant were assessed by ELISA. ResultsThe transfection of miR-33s mimic significantly increased the release of TNF-α,IL-6 and IL-1β(P<0.05). The expression of p38 MAPK protein was also significantly reduced(P<0.05). However,the pre-treatment of miR-33s inhibitor reversed the LPS-induced release of TNF-α,IL-6,and IL-1β,and the expression of p38 MAPK protein of THP-1 cells. ConclusionmiR-33s may play an important role in the regulation in inflammatory factors released from THP-1 cells by targeting p38 MAPK.
Objective To investigate the changes and significance of serum inflammatory factors in coronary heart disease ( CHD) patients with obstructive sleep apnea-hypopnea syndrome ( OSAHS) , and the treatment effects of continuous positive airway pressure( CPAP) . Methods A total of 76 CHD patients in Renmin Hospital of Wuhan University from October 2007 to October 2008 were enrolled. Polysomnography ( PSG) was performed in these CHD patients to identify if they were complicated by OSAHS. The levels of inflammatory factors including TNF-α, IL-6, high sensitive C-reactive protein ( hs-CRP) in serum were determined in the CHD patients and 23 normal subjects. The CHD patients with moderate-severe OSAHS ( AHI≥15 episodes/hour) were treated by Auto-CPAP for 3 months and all parameters above were measured again. Results There were 41 /76 ( 53. 9% ) of CHD patients had moderate-severe OSAHS and were treated with CPAP. The levels of TNF-α, IL-6 and hs-CRP were significantly higher in the CHD patients than those in the normal controls ( all P lt; 0. 01) , and were significantly higher in moderate-severe OSAHS patients than those in the non-OSAHS CHD patients. Auto-CPAP ventilation significantly decreased the levels of inflammatory factors in the CHD patients with moderate-severe OSAHS. Conclusions An obvious proinflammatory state is detected in CHD patients, and is aggravated with OSAHS. CPAP is a useful treatment for CHD patients with mediate to severe OSAHS.
Objective To investigate the influence of proteasome inhibitorMG-132 on inflammatory factors in COPD rats and its potential mechanism. Methods The COPD rat model was established by instillation of lipopolysaccharide and exposure to cigarette smoke. Then the rats were randomly divided into 4 groups( n = 12 in each group) , ie. a COPD model group, a COPD + MG-132 low concentration group ( 0. 05 mg·kg- 1·d - 1 ) , a COPD + MG-132 high concentration group( 0. 1 mg· kg- 1 · d - 1 ) , and a normal control group. The rats were injected intraperitoneally with different dose of MG-132 or normal saline. After 1 week and 4 weeks, 6 rats in each group were sarcrificed. Then the following parameters were determined including histopathological changes of lung tissue, and the concentrations of IL-1β, IL-6, IL-8 in serum and diaphragm via ELISA. Results The lung histopathological examination showed obvious emphysema and inflammatory infiltration in the COPD rats. These pathological changes were obviously ameliorated in two MG-132 treatment groups. The IL-1β, IL-6, and IL-8 levels in serumand diaphragmin the COPD model group were all significantly increased from1 week and 4 week than those in the normal control group( P lt;0. 05) .MG-132 down-regulated the expression of these inflammatory factors in a time-and dosedependent manner. The IL-1β, IL-6, and IL-8 levels in serum and diaphragm in the MG-132 low concentration group and high concentration group were all decreased compared with the COPD model group ( P lt; 0. 05) . Conclusion COPD is a systemic inflammatory disease which can be inhibited by the proteasome inhibitor MG-132 through suppressing inflammatory factors.
A new independent subtype CD4+ T cell which massively secreted interleukin-17 (IL-17) was found at the beginning of the 21st century, and thus it was named as T helper cell 17 (Th17 cell). With the progress of the research in recent years, Th17 cells were found to be widely involved in a variety of the human diseases such as autoimmune diseases, infections and tumors through secretion of IL-17. The relationship between Th17 cells, IL-17 and the occurrence, development and prognosis of lung cancer was reviewed.
Acute respiratory distress syndrome (ARDS) is the most common cause of acute respiratory failure. Extensive researches have been conducted for the pathophysiology of this disease, but the mortality rate remains high. Previous studies have found that catecholamines play an important role in acute lung injury, and newly discover prompted that upregulation of phagocyte-derived catecholamines augmented the acute inflammatory response in acute lung injury which provides a new way of thinking. In the current review, we describe the mechanism of the phagocyte-derived catecholamines augmenting the acute lung injury.