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The benefit of laparoscopic complete mesocolic excision (LCME) is conflicting in terms of short-term outcomes when compared with laparoscopic non-complete mesocolic excision (LNCME) for right colon cancer. Herein, we performed a meta-analysis to elucidate the safety and efficacy of LCME and LNCME. We searched PubMed, Embase, and the Cochrane Library databases for studies addressing the effects of LCME versus LNCME up to February 2021. Randomized controlled trials (RCTs) and retrospective studies which compared LCME with LNCME were included. Two RCTs and 6 retrospective studies with a total of 1925 patients met our search criteria and were assessed. 922 patients underwent LCME and 1003 patients underwent LNCME. Although LCME was associated with a longer operative time (weighted mean difference [WMD]: 14.26 min; 95% confidence interval [CI] 4.56 to 23.96; p = 0.004), patients in this group might benefit from less intraoperative blood loss (WMD: 11.30 ml; 95%CI −19.93 to −2.68; p = 0.01), a greater number of harvested lymph nodes (WMD: 6.82; 95%CI 4.04 to 9.59; p

Introduction The benefit of transanal total mesorectal excision (TaTME) for mid and low rectal cancer is conflicting. Aim To assess and compare the short-term outcomes of TaTME with conventional laparoscopic total mesorectal excision (LaTME) for middle and low rectal cancer. Material and methods We searched PubMed, Embase and Cochrane Library databases for studies addressing TaTME versus conventional LaTME for rectal cancer between 2008 and December 2018. Randomized controlled trials (RCTs) and retrospective studies which compared TaTME with LaTME were included. Results Twelve retrospective case-control studies were identified, including a total of 899 patients. We did not find significant differences in overall intraoperative complications, blood loss, conversion rate, operative time, overall postoperative complication, anastomotic leakage, ileus, or urinary morbidity. Also no significant differences in oncological outcomes including circumferential resection margin (CRM), positive CRM, distal margin distance (DRM), positive DRM, quality of mesorectum, number of harvested lymph nodes, temporary stoma or local recurrence were found. Although the TaTME group had better postoperative outcomes (readmission, reoperation, length of hospital stay) on average, the difference did not reach statistical significance. Conclusions Transanal total mesorectal excision offers a safe and feasible alternative to LaTME although the clinicopathological features were not superior to LaTME in this study. Currently, with the lack of evidence on benefits of TaTME, further evaluation of TaTME requires large randomized control trials to be conducted.

Background Inflammation plays an important role in thrombus formation, and Sirtuin 1 (SIRT1) negatively regulates inflammation via deacetylating nuclear factor-kappa B. However, the relationship between SIRT1-regulated inflammation and deep vein thrombosis (DVT) is still unknown. Objective The aim of this study was to investigate whether SIRT1 plays a critical role in inferior vena cava (IVC) stenosis-induced DVT. Materials and Methods Thrombus weight and histopathologic analysis of IVC were evaluated at different time points after IVC stenosis in rats. Serum levels of inflammatory cytokines and protein expressions of SIRT1, acetylated p65 (Ace-p65), phosphorylated p65 (p-p65) and tissue factor (TF) in thrombosed IVC were assessed. Besides, the effects of resveratrol (RES, a SIRT1 agonist) and EX527 (a selective SIRT1 inhibitor) on DVT were evaluated. Results Thrombus weight was increased from 1 to 3 days after IVC stenosis, and then was decreased afterwards. Leukocytes infiltration appeared and serum levels of cytokines were significantly increased in rats of IVC stenosis. SIRT1 protein expression was significantly down-regulated at 1 hour and 1 day after stenosis, while p-p65, Ace-p65 and TF protein expressions appeared a contrary trend. RES reduced thrombus weight, leukocytes infiltration, levels of tumour necrosis factor-α and interleukin-1β and protein expressions of Ace-p65 and TF as well. Moreover, RES significantly increased the protein and messenger ribonucleic acid expressions of SIRT1, while EX527 abolished the protective effects of RES. Conclusion SIRT1 activation attenuated IVC stenosis-induced DVT via anti-inflammation in rats. Therefore, SIRT1 may be a potential therapeutic target that could ameliorate DVT.

Background Deep vein thrombosis (DVT) is a kind of blood stasis syndrome. Spatholobi Caulis (SC) has been widely used for the treatment of blood stasis syndrome in China, but the underlying mechanism remains poorly understood. Purpose The aim of present study was to investigate the anti-DVT mechanism of Spatholobi Caulis dispensing granule (SCDG). Study design/methods A rat model of inferior vena cava (IVC) stenosis-induced DVT and a cell model of oxygen-glucose deprivation (OGD) were performed. Rats were orally administered with SCDG solution once daily for seven consecutive days. IVC stenosis-induced DVT was operated on the sixth day. Thrombi were harvested and weighed on the seventh day. Pathological changes were observed by hematoxylin-eosin (HE) staining. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β of serum were analyzed by enzyme-linked immunosorbent assay. C-reactive protein (CRP) was measured with turbidimetric immunoassay. Protein expressions in thrombosed IVCs and/or OGD-stimulated EA. hy926 cells were evaluated by western blot and/or immunofluorescence analyses. Results SCDG dramatically decreased thrombus weight. SCDG decreased tissue factor (TF) protein expression, inflammatory cells influxes in thrombosed vein wall and serum levels of inflammatory cytokines and CRP. Further, SCDG up-regulated Sirtuin 1 (SIRT1) protein expression and down-regulated acetylated-NF-κB p65 (Ace-p65) protein expression. Moreover, SCDG up-regulated nuclear factor-erythroid 2 related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) protein expressions, and down-regulated phosphorylated-NF-κB p65 (p-p65) protein expression. In the OGD cell model, SCDG medicated serum decreased the protein expression of TF. SCDG medicated serum enhanced SIRT1 protein expression and reduced Ace-p65 nuclear protein expression. SCDG medicated serum promoted protein expressions of nuclear Nrf2 and total HO-1, and inhibited translocation of p65. Furthermore, inhibiting SIRT1 and Nrf2 reversed the protective effect of SCDG medicated serum on OGD-induced EA. hy926 cells. Conclusion SCDG may prevent DVT through antiinflammation via SIRT1 and Nrf2.

Background Dry age-related macular degeneration (dAMD) leads to serious burden of visual impairment and there is no definitive treatment. Previous studies have showed that naringenin (NAR) significantly increased electroretinography (ERG) c-wave in sodium iodate (NaIO3)-treated rats and viability of NaIO3-treated ARPE-19 cells. But the underlying mechanism is still unknown. Purpose We tested the hypothesis that anti-oxidation mediated by Sirtuin 1 (SIRT1) was important to the protective effect of NAR on dAMD. Study design/Methods NaIO3-induced mice retinopathy and ARPE-19 cells injury models were established. In vivo, the protective effect of NAR eye drops on retina was evaluated by flash ERG (FERG) recording and histopathological examination. In vitro, viability of ARPE-19 cells, and the levels of lactic dehydrogenase (LDH), reactive oxygen species (ROS) and carbonyl protein were detected. Protein expression of SIRT1 was analyzed by immunochemical staining, immunofluorescence and western blotting. Results NAR eye drops improved retinal function and morphology and normalized the protein expression of SIRT1 in mice exposed to NaIO3. NAR promoted the survival of ARPE-19 cells in a concentration-dependent manner. NAR up-regulated SIRT1 protein expression, and decreased levels of ROS and carbonyl protein. Moreover, EX527, a selective inhibitor of SIRT1, abolished the effects of NAR on the cell viability and ROS. In addition, SRT1720, a selective agonist of SIRT1, improved the viability of cells and suppressed the production of ROS. Conclusion Our findings indicate that SIRT1-mediated anti-oxidation contributes to the protective effect of NAR eye drops on dAMD.

Background The pathogenesis of deep vein thrombosis (DVT) is incompletely understood, requiring reliable animal models. Inferior vena cava (IVC) stenosis model mimics human DVT. Objective To provide optimal conditions for establishing a rat model of IVC stenosis-induced DVT. Methods Effects of suture, and body weight, sex and side branches of rats on the IVC stenosis model were evaluated. 1 d after modeling, the weight and length of thrombosed IVCs and side branch distance were measured. Histopathological change and leukocytes influxes were observed by hematoxylin and eosin staining. Ly-6G-positive neutrophils were located by immunofluorescence. A multiple regression linear model was then built. Results IVCs stenosed with silk or monofilament sutures presented no difference in leukocyte influxes. Thrombus of 220−340 g rats was significantly heavier than that of 180−220 g rats. Although no statistic difference was found in thrombus weight between male and female rats weighing 180−260 g, males weighing 260−300 g formed larger thrombi than weight-matched females. Thrombus weight and length of rats except 180−220 g females was not impacted by side branch ligation and side branch distance. The regression model showed that sex and body weight were key factors affecting thrombus weight. Conclusions Male and female rats weighing 220−260 g are more suitable for establishing a model of DVT induced by stenosing IVC with silk and without side branch ligation.

Background Whitmania pigra Whitman (W pigra), a traditional Chinese medicine, has functions of breaking stagnant and eliminating blood stasis. The aim of this study was to investigate the underlying mechanism of W pigra against deep vein thrombosis (DVT). Methods A rat model of DVT induced by inferior vena cava stenosis was successfully established. Rats were administered vehicle (saline solution, p.o.), three doses of W pigra aqueous extract (34.7, 104.2, or 312.5 mg crude W pigra/kg, p.o.), heparin (200 U/kg, i.v.), or clopidogrel (25 mg/kg, p.o.) once daily for 2 d. Thrombus weight and histopathological changes were examined. Blood samples were collected to determine blood cell counts, blood viscosity, blood coagulation, blood fibrinolysis, serum levels of interleukin-1β, and tumor necrosis factor-α. Protein expressions of Sirtuin1 (SIRT1), acetylated p65 (Ace-p65), and phosphorylated p65 (p-p65) were determined by Western blot. Furthermore, SIRT1-specific inhibitor EX527 was applied to confirm the role of SIRT1 in the antithrombotic effect of W pigra. Results W pigra significantly decreased thrombus weight. W pigra had no effects on blood cell counts, whole blood viscosity, blood coagulation, blood fibrinolysis. However, it reduced tissue factor protein expression in the vein wall and thrombus. Moreover, it sharply increased SIRT1 protein expression and decreased leukocytes recruitment in the thrombus and vein wall, serum levels of interleukin-1β and tumor necrosis factor-α, and protein expressions of Ace-p65 and p-p65. Furthermore, the antithrombotic effect of W pigra was significantly abolished by EX527. Conclusions Aqueous extract of W pigra effectively reduced DVT burden by inhibiting inflammation via SIRT1/nuclear factor-kappa B signaling pathway.

Ethnopharmacological relevance Danhong Huayu Koufuye (DHK), a compound traditional Chinese medicine, is composed of Salvia miltiorrhiza radix (Salvia miltiorrhiza Bge.), Angelicae Sinensis radix (Angelicae Sinensis (Oliv.) Diels.), Chuanxiong rhizoma (Ligusticum chuanxiong Hort.), Persicae semen (Prunus persica (L.) Batsch), Carthami flos (Carthamus tinctorius L.), Bupleuri radix (Bupleurum chinense DC.) and Aurantii fructus (Citrus aurantium L.). DHK prevents deep vein thrombosis (DVT) through antiinflammation. However, the antiinflammatory mechanism of DHK is still unknown. Objective The aim of this study was to evaluate whether DHK prevented venous thrombosis through antiinflammation via Sirtuin 1 (SIRT1)/NF-κB signaling pathway. Methods Inferior vena cava (IVC) stenosis-induced DVT rat model was established. Rats were administered with DHK (1.6, 3.2 or 6.4 mL/kg/d, p.o.), heparin (200 U/kg/d, i.v.), clopidogrel (25 mg/kg/d, p.o.), resveratrol (50 mg/kg/d, p.o.) or vehicle (p.o.) once daily for two days. Blood coagulation, blood fibrinolysis, blood viscosity, blood cell counts and platelet activity were evaluated. Serum levels of inflammatory cytokines were analyzed by enzyme-linked immunosorbent assay. Pathological changes were observed by hematoxylin-eosin (HE) staining. Protein expressions in thrombosed IVCs were evaluated by Western blot and/or immunofluorescence analyses. SIRT1 mRNA expression was analyzed by real-time quantitative polymerase chain reaction. Besides, SIRT1-specific inhibitor EX527 was pretreated to confirm the role of SIRT1/NF-κB signaling pathway in the antithrombotic effect of DHK. Results DHK remarkably prevented DVT. DHK had no effects on blood coagulation, blood fibrinolysis, blood viscosity, blood cell counts or platelet activity. But DHK significantly up-regulated protein and mRNA expressions of SIRT1, and reduced leukocytes infiltration into thrombus and vein wall, serum levels of inflammatory cytokines, and protein expressions of acetylated p65 (Ace-p65), phosphorylated p65 (p-p65) and tissue factor (TF). Moreover, the antithrombotic effect of DHK was significantly abolished by EX527. Conclusion DHK may prevent DVT by inhibiting inflammation via SIRT1/NF-κB signaling pathway.

Danhong Huayu Koufuye (DHK), a traditional Chinese prescription, is used to treat central retinal vein occlusion clinically. We previously reported that DHK prevented diabetic retinopathy (DR) in rats. Moreover, we found that it protected endothelial cells from hyperglycemia-induced apoptosis through antioxidation and anti-inflammation. Here, we investigated whether antioxidative and anti-inflammatory activities of DHK contributed to its therapeutic effect on DR in streptozotocin- (STZ-) induced diabetic rats. DHK significantly blocked the breakdown of the blood-retinal barrier (BRB) and increased the thickness of the inner nuclear layer (INL), as well as suppressed the swelling of the ganglion cell layer (GCL) in diabetic retinas. DHK remarkably increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in plasma, and decreased serum level of nitric oxide (NO). Moreover, DHK markedly reduced the serum levels of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule-1 (ICAM-1). Furthermore, DHK significantly downregulated protein expressions of VEGF and inducible NO synthase (iNOS) and mRNA expression of ICAM-1 in retinas. These results suggest that the antioxidative and anti-inflammatory activities of DHK may be important mechanisms involved in the protective effect of DHK on DR in STZ-induced diabetic rats.

It has been shown that oxidative damage and inflammation caused by hyperglycemia in endothelial cells are key factors triggering diabetic vascular complications. The aim of the present study was to investigate the antioxidant and anti‑inflammatory effects of Danhong Huayu Koufuye (DHK)‑medicated serum on high glucose (HG)‑induced injury in endothelial cells, and examine its underlying mechanisms. EA. hy926 cells were treated with normal glucose, HG, or HG with DHK‑medicated serum. Cell viability was assessed using the MTT method. Apoptosis was detected using flow cytometry. Intracellular reactive oxygen species (ROS) levels were measured using the 2',7'‑dichlorodihydrofluorescein method. Cell culture supernatant was collected for detecting the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA). The protein expression levels of intercellular adhesion molecule‑1 (ICAM‑1), nuclear factor‑κB (NF‑κB), hypoxia‑inducible factor‑1α (HIF‑1α) and vascular endothelial growth factor (VEGF) were determined using western blot analysis. The results revealed that DHK‑medicated serum accelerated the proliferation and inhibited the apoptosis of cells treated with HG (P

Danhong huayu koufuye (DHK) has traditionally been used clinically for a long time in China. This study was to evaluate the effect of DHK in treating deep vein thrombosis (DVT) in rats and explore its possible mechanism.Forty-eight Sprague-Dawley rats were divided into four groups, performed with incomplete inferior vena cava ligation to induce DVT, and orally administered with DHK (3.20 mg/kg/d), warfarin (2.00 mg/kg/d), or vehicle for 7 days. The involved inferior vena cava and thrombi were collected and measured in size. The tissue specimens were performed for routine histopathologic evaluation and immunohistochemical staining with tissue factor and matrix metalloproteinases-9. Blood samples were collected for detecting coagulation function, blood cell count, and the levels of interleukin-6 and tumor necrosis factor-α.The treatment of DHK markedly reduced the size of thrombi by 49.26%, and the vein wall thickness by 47.86%. The recanalization rate was significant higher in the DHK-treated group than the vehicle-treated group (26.34 ± 6.53% versus 15.91 ± 3.93%, P0.01). Comparing to vehicle control, DHK significantly reduced neutrophils (P0.05) and lymphocytes (P0.05), serum tumor necrosis factor-α level (4.90 ± 1.14 pg/mL versus 6.60 ± 1.62 pg/mL, P0.01), and the expression of matrix metalloproteinases-9 and tissue factor (P0.05) in thrombi.DHK effectively prevented DVT through anti-inflammatory action in rats.