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Background Although several prediction models for the occurrence of clinically relevant postoperative pancreatic fistula after laparoscopic pancreatoduodenectomy exist, most were established using Western cohorts. The utility of these models using a Chinese cohort has not been validated widely. The aim of the study was to validate the original Fistula Risk Score, the alternative Fistula Risk Score, and the updated alternative Fistula Risk Score for patients undergoing laparoscopic pancreatoduodenectomy in a large-scale Chinese cohort externally. Methods Three clinically relevant postoperative pancreatic fistula risk models were selected for external validation with our database. Primary outcome was grade B/C postoperative pancreatic fistula (clinically relevant postoperative pancreatic fistula). Performance was measured based on sensitivity, specificity, positive and negative predictive value, positive and negative likelihood ratio, and area under the curve. The original Fistula Risk Score was also compared with the alternative Fistula Risk Score and the updated alternative Fistula Risk Score. Results Of the 400 patients who underwent laparoscopic pancreatoduodenectomy, 60 (15.00%) developed clinically relevant postoperative pancreatic fistula. For the original Fistula Risk Score, the alternative Fistula Risk Score, and the updated alternative Fistula Risk Score, the sensitivity was 65.00%, 90.00%, and 90.00%; the specificity was 43.53%, 44.12%, and 37.65%; the positive predictive value was 16.88%, 22.13%, and 20.30%; the negative predictive value was 87.57%, 96.15%, and 95.52%; positive likelihood ratio was 1.151, 1.611, and 1.443; negative likelihood ratio was 0.804, 0.227, and 0.266, respectively. The area under the curve values were 0.608 (95% confidence interval 0.573–0.649), 0.733 (95% confidence interval 0.692–0.797), and 0.720 (95% confidence interval 0.688–0.763) on the original Fistula Risk Score, the alternative Fistula Risk Score, and the updated alternative Fistula Risk Score (P Conclusion The alternative Fistula Risk Score and the updated alternative Fistula Risk Score had similarly good predictive utility. The original Fistula Risk Score performed less well. We recommended to use the alternative Fistula Risk Score and the updated alternative Fistula Risk Score to predict occurrence of clinically relevant postoperative pancreatic fistula after laparoscopic pancreatoduodenectomy when applied to a Chinese cohort.

Background Enhanced recovery after surgery (ERAS) programs have achieved promising results in many surgical specialties. However, uncertainty still remains regarding the effect of ERAS on hip fractures. The objective of this review was to investigate the clinical prognosis of ERAS programs in terms of (1) hospital-related endpoints (time to surgery [TTS], length of stay [LOS]), (2) readmission rate, (3) complications, and (4) mortality. Methods Published literature was searched in the PubMed, EMBASE, and Cochrane Library databases. All of the included studies met the inclusion criteria. The primary outcomes were TTS and LOS. The secondary outcomes included the 30-day readmission rate, overall complication rate, specific complication rate (delirium and urinary tract infection), and 30-day and 1-year mortality. Language was restricted to English. The data analysis was carried out by Review Manager 5.3. Results A total of 7 published studies (9869 patients) were finally included, and these were all cohort studies. The meta-analysis showed that the TTS, LOS, and overall complication rate were significantly reduced in the ERAS group compared with the control group (p < 0.01). Moreover, no significant change was found in the 30-day readmission rate or 30-day and 1-year mortality. Conclusions ERAS significantly decreases the TTS, LOS, and complication rate without increasing readmission rate and mortality, which adds to the evidence that the implementation of ERAS is beneficial to patients undergoing hip fracture repair surgeries.

CD160 is an Ig-like glycoprotein expressed by the majority of circulating natural killer cells and γδ T cells. Whether CD160 could regulate CD8+ T-cell functions remains unknown. In this study, we investigated the effects of CD160 on CD8+ T cells in pancreatic cancer. First, we found that the frequency of PD-1+ cells was comparable between CD160+ and CD160-CD8+ T cells, with the former presenting significantly higher PD-1 expression level. In contrast, the frequency of TIM-3+ cells was higher among CD160+ cells but the expression level was comparable between CD160+ and CD160-CD8+ T cells. The IFN-γ and IL-2-expressing CD8+ T cells, directly ex vivo, were highly enriched in the CD160+ subset. However, when CD160+ and CD160-CD8+ T cells were stimulated, the proliferation levels of CD160+ and CD160- cells were initially comparable, but were significantly lower in CD160+CD8+ T cells than in CD160-CD8+ T cells later on. The IFN-γ and IL-2 transcription levels were initially higher in CD160+CD8+ T cells, but eventually reduced in CD160+CD8+ T cells compared to CD160-CD8+ T cells. Also, CD160+CD8+ T cells presented lower cytotoxic capacity than CD160-CD8+ T cells. Interestingly, we observed that tumor-infiltrating CD8+ T cells were significantly enriched with the CD160+ subset in pancreatic cancer patients. In addition, patients with higher frequencies of tumor CD160+CD8+ T cells presented lower survival. Overall, these data demonstrated that tumor-infiltrating CD8+ T cells were enriched with the CD160+ subset in pancreatic cancer, with active effector responses directly ex vivo but limited potential for further activation.

Background The Cadherin-11 and PI3K/Akt pathway are increasingly recognized as the potential therapeutic target of osteoarthritis (OA) synovitis. The study aimed to investigate the role of PI3K/Akt signaling pathway in the expression of Cadherin-11 and migration and invasive capacity of fibroblast-like synoviocytes (FLS) of OA patients under stimulation of TNF-α and to explore the effect of the PI3K/Akt inhibitor and Cadherin-11 antibody in the therapy of the collagenase-induced osteoarthritis (CIOA) mice. Methods FLS were primarily cultured from synovium of osteoarthritic patients during total knee arthroplasty. Under the simulation of TNF-α, with or without PI3K/Akt inhibitor LY294002, Cadherin-11 expression was detected by real-time PCR and Western blot, as well as the migration and invasive capacity changes of OA FLS. Cadherin-11 antibody was injected intraarticularly or LY294002 was injected intraperitoneally in CIOA mice to evaluate the changes of synovitis score, cartilage damage, and Cadherin-11 expression. Results TNF-α stimulation increased Cadherin-11 expression at mRNA and protein level in OA FLS and also increased the phosphorylation-dependent activation of Akt. PI3K inhibitor LY294002 attenuated TNF-α-induced overexpression of Cadherin-11 and decreased the invasive capacity of OA FLS. Intraperitoneal injection of PI3K inhibitor LY294002 could decrease the Cadherin-11 protein expression in synovium of CIOA mice, although it has no significant inhibitory effect on synovitis and cartilage damage. Intraarticular injection of Cadherin-11 antibody attenuated the synovitis and cartilage damage in the CIOA joints and decreased Cadherin-11 expression in the synovial lining. Conclusions PI3K/Akt pathway was associated with TNF-α-induced activation of OA FLS, which may involve in the pathogenesis of osteoarthritis. Anti-Cadherin-11 therapy in CIOA mice could attenuate the pathological changes of OA joints.

Background and objective: ITGA3 is a cell surface adhesion protein that interacts with extracellular matrix proteins which function in cancer metastasis. We examined the relationship of pancreatic ITGA3 expression with the clinical and pathological characteristics of patients with pancreatic cancer. Methods: Data mining was used to analyze pancreatic cancer data from The Cancer Genome Atlas database. A Chi squared test was used to evaluate correlations of ITGA3 expression with clinical and pathological parameters. Receiver operating characteristic (ROC) analysis was used to evaluate the diagnostic performance of ITGA3 expression. Survival analysis and Cox regression analysis were used to examine the prognostic value of ITGA3 expression. Gene Set Enrichment Analysis (GSEA) was used to identify signaling pathways related to ITGA3 expression. Results: Pancreatic expression of ITGA3 was greater in patients with pancreatic cancer than those without cancer, and was also associated with histological type, histological grade, stage, T classification, vital status, and relapse. ROC analysis indicated that ITGA3 had significant diagnostic value, in that high expression correlated with poor overall survival and relapse-free survival, especially in patients with early-stage cancer. Cox analysis indicated that high ITGA3 expression was an independent prognostic factor for pancreatic cancer. GSEA analysis identified 9 signaling pathways that were enriched in the presence of high ITGA3 expression. Conclusion: Expression of ITGA3 can be used as a diagnostic and prognostic biomarker in pancreatic cancer.

Studies have indicated that oxidative stress plays a crucial role in the development of Parkinson’s disease (PD) and other neurodegenerative conditions. Research has also revealed that nuclear factor erythroid 2-related factor 2 (Nrf2) triggers the expression of antioxidant genes via a series of antioxidant response elements (AREs), thus preventing oxidative stress. Thymoquinone (TQ) is the bioactive component of Nigella sativa, a medicinal plant that exhibits antioxidant and neuroprotective effects. In the present study we examined whether TQ alleviates in vivo and in vitro neurodegeneration induced by 1-methyl-4-phenylpyridinium (MPP+) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by acting as an activator of the Nrf2/ARE cascade. We showed that TQ significantly reduced MPP+-mediated cell death and apoptosis. Moreover, TQ significantly elevated the nuclear translocation of Nrf2 and significantly increased the subsequent expression of antioxidative genes such as Heme oxygenase 1 (HO-1), quinone oxidoreductase (NQO1) and Glutathione-S-Transferase (GST). The application of siRNA to silence Nrf2 led to an abolishment in the protective effects of TQ. We also found that the intraperitoneal injection of TQ into a rodent model of PD ameliorated oxidative stress and effectively mitigated nigrostriatal dopaminergic degeneration by activating the Nrf2-ARE pathway. However, these effects were inhibited by the injection of a lentivirus wrapped Nrf2 siRNA (siNrf2). Collectively, these findings suggest that TQ alleviates progressive dopaminergic neuropathology by activating the Nrf2/ARE signaling cascade and by attenuating oxidative stress, thus demonstrating that TQ is a potential novel drug candidate for the treatment of PD.

Triptolide (TPL) is a diterpenoid triepoxide with broad antitumor efficacy, while lack of mechanism of action, severe systemic toxicity, and poor water solubility of TPL limited its usage. To unveil the mechanism of action and improve the pharmaceutical properties of TPL, here we explored the molecular mechanism of TPL and then fabricated TPL-loaded membrane protein-chimeric liposomes (TPL@MP-LP) and tested its anticancer efficacy against hepatocellular carcinoma (HCC). CCK8 assay, colony formation assay, EdU assay, and flow cytometry were used to examine the activity of TPL. RNA sequence and gain-and-loss of function assays were used to explore the molecular mechanisms. TPL@MP-LP was characterized by size, zeta potential, polydispersity index, and transmission electron microscopy. Cellular uptake and cell viability assay were performed to evaluate the internalization and anticancer efficacy of TPL@MP-LP in vitro. Biodistribution and in vivo antitumor efficacy of TPL@MP-LP were evaluated on orthotopic HCC mice models. TPL robustly inhibited HCC cells by inducing cell proliferation arrest, apoptosis via the mitochondrial pathway, and necroptosis via RIPK1/RIPK3/MLKL signaling. TPL was successfully loaded into MP-LP, with a drug-loading capacity of 5.62 ± 0.80%. MP-LP facilitated TPL internalization and TPL@MP-LP exerted enhanced anticancer efficacy against Huh7 cells. TPL@MP-LP showed targeting ability to the tumor site. More importantly, TPL@MP-LP treatment suppressed tumor growth but showed minimal damage to liver and renal functions. TPL exerted anticancer effects on HCC via inducing cell proliferation arrest, apoptosis, and necroptosis, and the MP-LP might be a promising delivery strategy to improve the antitumor efficacy while mitigating toxicity of TPL for HCC therapy.

Background Angioleiomyoma is a very rare benign solitary soft tissue neoplasm originating from smooth muscle layer of blood vessels. The tumor is usually located in the subcutis or the superficial fasciae, but less often in the deep fasciae, especially rare in the knee joint cavity. Diagnosis is frequently delayed or misdiagnosed as loose body or anterior knee pain because of its rare occurrence and poor awareness of physicians. Few studies have presented intra-articular angioleiomyoma and such cases become rarer and more difficult to diagnose when it presents as loose body. Case presentation Two patients, a middle-aged man and an old woman, presented to our outpatient clinic with persistent anterior knee pain and both of them suffered from a solitary mass in the right knee that had slowly enlarged. One of two patients showed negative in the routine radiographic imaging and the other showed a “loose body” beside the lateral femoral condyle in the knee. MRI showed both a well-demarcated intra-articular mass of isointense signal to muscle on T1-weighted images and heterogeneous intensity on T2-weighted images. Their tumors were excised under arthroscopy finally, with the pathological results revealed vascular leiomyomas. They both recovered well with pain free after operation and no signs of recurrence were seen at the 7-year follow-up. Conclusions This case report illustrates the atypical locations of angioleiomyoma in the knee joint should arouse our attention and be included in the differential diagnosis of nodular lesions mimicking loose bodies.

Peripheral nerve injury (PNI) is an unresolved medical problem with limited therapeutic effects. Epineurium neurorrhaphy is an important method for treating PNI in clinical application, but it is accompanied by inevitable complications such as the misconnection of nerve fibers and neuroma formation. Conduits small gap tubulization has been proved to be an effective suture method to replace the epineurium neurorrhaphy. In this study, we demonstrated a method for constructing peripheral nerve conduits based on the principle of chitosan acetylation. In addition, the micromorphology, mechanical properties and biocompatibility of the chitin nerve conduits formed by chitosan acetylation were further tested. The results showed chitin was a high-quality biological material for constructing nerve conduits. Previous reports have demonstrated that mesenchymal stem cells culture as spheroids can improve the therapeutic potential. In the present study, we used a hanging drop protocol to prepare bone marrow mesenchymal stem cell (BMSCs) spheroids. Meanwhile, spherical stem cells could express higher stemness-related genes. In the PNI rat model with small gap tubulization, BMSCs spheres exhibited a higher ability to improve sciatic nerve regeneration than BMSCs suspension. Chitin nerve conduits with BMSCs spheroids provide a promising therapy option for peripheral nerve regeneration.

Small Nucleolar RNA Host Gene (SNHG16) is a novel cancer-related long noncoding RNA (lncRNA) and functions as an oncogene in a variety of cancers. Nonetheless, the expression patterns, biological function, and potential mechanisms in SNHG16 in pancreatic cancer (PC) remain rarely known. An increase in expression of SNHG16 in PC samples against adjacent normal tissues was shown here. Increased SNHG16 was linked intimately to the tumor-node-metastasis (TNM) stage, distant metastasis, tumor differentiation, and poor overall survival. Loss-of-function experiments revealed that SNHG16 knockdown suppressed the proliferation, formation of colonies, ability to migrate and invade in vitro, along with a lowered growth of the tumor in a mouse model. Mechanistically, SNHG16 might serve as a sponge competitive endogenous RNA (ceRNA) for miR-218-5p, thereby playing a role in regulating the expression of high mobility group box 1 (HMGB1) expression, a known direct miR-218-5p target in PC cells. These results provide novel insight into PC tumorigenesis and suggest that SNHG16 could serve as a likely therapeutic intervention in PC.

A growing body of evidence suggests that microRNA-363 (miR-363) plays crucial roles in tumor progression, development and metastasis, and confer resistance to chemotherapeutic drugs in several types of cancers. However, the biological function and underlying molecular mechanism of miR-363 in hepatocellular carcinoma (HCC) have not been fully elucidated. In the present study, we investigated the biological function and mechanism of miR-363 in the regulation of HCC progression. We found that miR-363 was downregulated in HCC cell lines and tissues, and a low expression level of miR-363 was associated with tumor differentiation, TNM stage and lymph node metastasis. Forced overexpression of miR-363 significantly suppressed HCC cell proliferation, migration, invasion and decreased epithelial‑mesenchymal transition (EMT) in vitro, as well as inhibited tumor growth in vivo. Analysis of the underlying mechanisms revealed that miR-363 regulated E2F transcription factor 3 (E2F3) expression by directly targeting its 3' untranslated region. E2F3 overexpression partially attenuated the tumor-suppressive effects of miR-363 in HCC cells. In addition, E2F3 expression was upregulated in the HCC tissues, and was negatively correlated with the level of miR-363 in human HCC tissues. Taken together, these results revealed that miR-363 is involved in HCC growth and invasion and functions as a tumor suppressor by negatively regulating E2F3.

The miR‑222 cluster has been demonstrated to function as oncomiR in human hepatocellular carcinoma (HCC). miR‑222 confers chemotherapy drug resistance in various cancers, including HCC. However, the effects and mechanisms by which miR‑222 regulates liver tumorigenicity and confers sorafenib (SOR) resistance remain unclear. Here we first investigated the miR‑222 effect on proliferation, cell cycle, apoptosis, migration and invasion of HCC. Our results demonstrated that miRNA inhibitors specially targeting miR‑222 significantly suppressed cellular proliferation, migration, invasion and G1/S transition of the cell cycle, and induced cell apoptosis in HepG2 cells. In addition, we investigated whether miR‑222 confers SOR resistance in HepG2 cells to explore it roles in acquisition of drug resistance. The results showed that miR‑222 inhibitors induced sensitivity to the antitumor effect of sorafenib in human HepG2 cells. Importantly, our study also showed that miR‑222 could regulate the expression of phosphorylation PI3K and AKT, which might contribute to miR‑222 conferred SOR resistance in HepG2 cells. In conclusion, this study demonstrates that miR‑222 can promote cell proliferation, migration and invasion, and decrease cell apoptosis, as well as enhance the resistance of HCC cells to sorafenib miR‑222 through activating the PI3K/AKT signaling pathway.

Objective: This retrospective study compared the advantages and disadvantages of iodine-125 (125I) seed implantation and pancreaticoduodenectomy (PD) in the treatment of pancreatic cancer. Methods: Patients with diagnosed pancreatic cancer who were treated with 125125I seed implantation (30 patients) or PD (30 patients) in our hospital were evaluated for operative time, bleeding, liver function, time to first bowel movement and normal diet, survival, and medical costs. Results: Compared with patients who underwent PD, those given 125I seed implantation had significantly shorter operative time, less bleeding, higher albumin, shorter periods to bowel movement and normal diet, lower risk of complications, and lower medical costs (P < 0.001, each). The difference of bilirubin level, time to feeding, and median survival were not significant statistically between two treatment grouops. Conclusion: For pancreatic cancer patients for whom PD is not appropriate or who refuse PD, 125I seed implantation is a good option.

Retinal detachment typically occurs when the retina is pulled away from its normal position by blunt trauma. It has been estimated that traumatic retinal detachments account for 10-20% of all detachments. Understanding the mechanism of traumatic retinal detachment is helpful for ophthalmologists to make a more accurate diagnosis before the symptoms develop. A finite element eye model, validated through published data, was used to simulate traumatic retinal detachment. Retinal adhesive force was incorporated into the model using breakable bonded contact. Under BB impact, global deformation was divided into four stages: compression, decompression, overshooting and oscillation. Shockwave propagation in the retina produced high strain in the retina. For an impact speed of 50 m/s, the peak strain of 0.138 in ora serrata exceeded the specified threshold for retinal break. When the eye was decompressed, negative pressure occurred around and anterior to the equator, with a minimum of -663 kPa, leading to retinal detachment. The following relative inertia motions between the retina and its supporting tissue extended the detachment. In addition, the simulations of lower shear modulus of vitreous and increased retinal adhesive force also confirm that the extent of retinal detachment is determined by negative pressure and inertial motion. In conclusion, shockwave and negative pressure contribute to retinal detachment. Shockwave propagation in the retina leads to retinal break, while negative pressure and relative inertial motion could pull the retina away from the supporting tissue. The current work would help understand the basic mechanisms underlying blunt trauma.

Expression of miR-365 has been reported to be downregulated in hepatocellular carcinoma (HCC). However, the biological function and underlying mechanism of miR-365 in HCC growth and metastasis remain unclear. The aim of the present study was to explore the role of miR-365 in HCC progression. We found that miR-365 expression was downregulated in HCC tissues and cell lines. Further results showed that low expression of miR-365 was significantly associated with tumor-node-metastasis (TNM) stage and lymph node metastasis. Functional assays revealed that overexpression of miR-365 significantly inhibited cell proliferation, colony formation, migration and invasion of HCC cells in vitro, and suppressed tumor growth in vivo. Mechanistic investigations demonstrated that ADAM10 (a disintegrin and metalloproteinase 10) is a target of miR-365 in HCC. In addition, knockdown of ADAM10 in HepG2 cells significantly inhibited cell proliferation, colony formation, migration and invasion, which mimicked the suppressive effects induced by miR-365 overexpression. Restoration of ADAM10 expression partially reversed the suppressive effects mediated by miR-365 overexpression. Taken together, these results indicate that miR-365 functions as a tumor-suppressor in HCC through targeting ADAM10, and may serve as a promising candidate for therapeutic applications in HCC treatment.

Objective To detect the expression of cadherin-11 and its correlation with synovitis in osteoarthritis (OA), to explore the mechanism of over expression of cadherin-11 and its role in migratory or invasive capacity of fibroblast-like synoviocytes (FLS). Methods Synovitis severity was recorded according to Krenn’s scoring system in 25 osteoarthritis patients undergoing total knee arthroplasty. Cadherin-11 expression in OA synoviums and its correlation with synovitis score and systemic inflammation markers were explored. After induction with Interleukin-1 beta (IL-1β) or tumor necrosis factor-alpha (TNF-α),cadherin-11 expression on OA FLS was assessed by qPCR and western blot,the capacity of migration and invasion of OA FLS was tested by transwell assay, and matrix metalloproteinase-2 production was assessed with ELISA as cadherin-11 expression was up regulated after infection with cadherin-11 cDNA-containing lentivirus, also when cadherin-11 expression was knocked down after infection with cadherin 11 shRNA containing lentivirus. Results Cadherin-11 expression in OA synovium showed significant differences among different grades of synovitis. Cadherin-11 in the lining layer was positively correlated with hyperplasia of the lining layer, density of the resident cells, inflammatory infiltrate, total synovitis score and D-dimer. Cadherin-11 in the sublining layer was positively correlated with the density of the resident cells, inflammatory infiltrate, total synovitis score and erythrocyte sedimentation rate. IL-1β or TNF-α could up-regulate cadherin-11 expression on OA FLS at transcriptional and protein level. Over expression of cadherin-11 increased migratory or invasive capacity of OA FLS, while cadherin-11 knock down reduced migratory or invasive capacity and MMP-2 production in OA FLS. Conclusion The over expression of cadherin-11 in osteoarthritis is positively correlated with synovitis severity, and can be driven by proinflammatory cytokines on OA FLS; cadherin-11 increases migratory or invasive capacity and MMP-2 production of fibroblast-like synoviocytes of osteoarthritis.

Sorafenib (SOR), a vascular endothelial growth factor receptor (VEGFR) inhibitor, is in wide clinical use for the treatment and prevention of liver cancer. However, extended SOR administration for hepatocellular carcinoma (HCC) induces drug resistance thereby limiting its efficacy and highlighting the need for improved therapeutic strategies. It has previously been demonstrated that knockout of a disintegrin and metalloproteinase 10 (ADAM10) via siRNA induced cancer apoptosis and decreased chemotherapy drug resistance. However, whether knockout of ADAM10 is able to decrease SOR resistance remains to be determined. Therefore, in the present study, the effect of siRNA-ADAM10 in combination with SOR was analyzed in HCC cell lines (HepG2) by inhibiting tumor growth and simultaneously reducing doses of SOR. Cell proliferation, apoptosis, migration, invasion and involvement in receptor signaling were determined after siRNA-ADAM10 was applied in combination with SOR treatment. Tumor growth ability in nude mice was also detected. The results showed that siRNA-ADAM10 in combination with SOR treatment in HCC cancer cells significantly suppressed proliferation, migration and invasion, and induced tumor apoptosis in vitro, and suppressed tumor growth in vivo. In addition, the results showed that knockout of ADAM10 by siRNA inhibited the constitutive phosphorylation of PI3K and AKT, which may contribute to the reduction of SOR resistance. Collectively, our experimental results indicate that knockout of ADAM10 by siRNA increased the SOR antitumor activity of liver cancer in vitro and in vivo, and that this additive combination is a promising drug candidate for treatment of HCC.

MicroRNAs (miRNAs) are a class of small non-coding RNAs and have critical roles in tumorigenesis and metastasis. A growing body of evidence showed that microRNA-133a (miR-133a) was downregulated and played tumor suppressor roles in gastric, colorectal, bladder, and lung cancer. However, the role and underlying molecular mechanism of miR-133a in hepatocellular carcinoma (HCC) remain unclear. In this study, we analyzed the expression of miR-133a in HCC tissues and HCC cell lines. We find that miR-133a was downregulated in HCC tissues and cell lines and that miR-133a expression negatively correlated with tumor differentiation (P

Background The purpose was to determine the influence of irrigation solution osmolarity on articular chondrocytes survival and metabolic state following mechanical injury. Methods Osteochondral explants were harvested from patients undergoing total knee arthroplasty for osteoarthritis and then cut through their full thickness to establish mechanical injury models. Cartilage explants were incubated in irrigation solutions (saline and balanced salt) with different osmolarities (180, 280, 380, 580 mOsm/L) for 2 h. The percentage of cell death (100 × number of dead cells/number of dead and live cells) was quantified with the laser confocal microscopy. The terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay was performed to detect apoptosis index of injured cartilage. The contents of proteoglycan elution were determined by spectrophotometer at 530 nm, and HIF-1α and type II collagen mRNA yields were quantified with real-time PCR. Results In situ dead chondrocytes were mainly localized to the superficial tangential region of injured cartilage edge after mechanical injury. The percentage of cell death was decreased, and proteoglycan elution was gradually reduced with the increasing of osmolarity. The apoptosis indices of TUNEL assay in different osmolarities had no significant difference (P = 0.158). HIF-1α and type II collagen mRNA yields were the least for chondrocytes exposed to 180 mOsm/L medium and were the greatest for chondrocytes exposed to 380 mOsm/L medium. Compared with the saline group, the cell death of superficial zone was significantly decreased (P = 0.001) and contents of proteoglycan elution were also significantly decreased (P = 0.045) in the balanced salt. HIF-1α (P = 0.017) and type II collagen (P = 0.034) mRNA yields in the chondrocytes exposed to the balanced salt were significantly more than the saline group. Conclusion The osmolarity of irrigation solutions plays an important role in the survival and metabolic state of chondrocytes following mechanical injury, and the chondrocyte death is not caused by apoptosis. Increasing osmolarity of irrigation solutions may be chondroprotective with decreasing the chondrocyte death, reducing inhibition of metabolism and proteoglycan elution, ultimately preventing cartilage degeneration and promoting integrative repair.