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The present study aimed to explore whether and how microRNA‑5580‑3p (miR‑5580‑3p) affected oral cancer (OC) cell phenotypes via regulation of laminin subunit γ2 (LAMC2). Bioinformatics analysis was used to identify miR‑5580‑3p/LAMC2, a novel interactome that, to the best of our knowledge, has not been studied previously in OC. In the present study, the expression levels of miR‑5580‑3p and LAMC2 were detected by reverse transcription‑quantitative PCR, while the protein expression levels of LAMC2 were identified using western blotting. To determine the effects of miR‑5580‑3p and LAMC2 in OC, a number of experiments, including Cell Counting Kit‑8, 5‑bromo‑2'‑deoxyuridine cell proliferation and wound healing migration assays, were performed using OC SCC‑4 and Cal‑27 cell lines. Additionally, luciferase reporter assays were employed to examine the interaction between miR‑5580‑3p and LAMC2 mRNA. The results demonstrated that miR‑5580‑3p expression was downregulated, while LAMC2 expression was upregulated in OC tissues and cell lines. In addition to the observation that miR‑5580‑3p promoted the malignant phenotypes of OC, it was also revealed that miR‑5580‑3p inhibited OC cell viability, proliferation and migration by suppressing LAMC2. Therefore, the present study suggested that miR‑5580‑3p and LAMC2 may be potential biomarkers and therapeutic targets for OC diagnosis and therapies in the future.

Acute kidney injury (AKI) is the most common complication of sepsis. The current incidence of sepsis is high (0.3% of total population) worldwide, and septic AKI may cause death in patients. Long non‑coding (lnc)RNAs serve important roles in the pathogenesis of AKI. Therefore, the present study investigated the mechanism underlying lncRNA plasmacytoma variant translocation 1 (PVT1)‑mediated regulation of pyroptosis in septic AKI. Septic kidney injury was induced in mice using the caecal ligation and puncture method, and lipopolysaccharide (LPS)‑induced HK‑2 cell models were also established. Haematoxylin‑eosin staining was performed to assess pathological alterations of kidney tissues in the mice. The levels of IL‑1β, IL‑18 and lactate dehydrogenase were determined by conducting ELISAs. Reverse transcription‑quantitative PCR was used to detect the expression levels of PVT1 and microRNA (miR)‑20a‑5p. To assess pyroptosis, the protein expression levels of nucleotide‑binding oligomerization domain‑like receptor protein 3 (NLRP3), IL‑1β, IL‑18, apoptosis‑associated speck‑like protein containing a CARD and cleaved caspase‑1 were measured via western blotting. Flow cytometry was performed to assess the rate of cell pyroptosis. Dual luciferase reporter assays were used to assess the binding relationships of PVT1/miR‑20a‑5p and miR‑20a‑5p/NLRP3. PVT1 expression was significantly increased, whereas miR‑20a‑5p expression was significantly decreased in sepsis model mice and LPS‑induced HK‑2 cells compared with sham mice and control HK‑2 cells, respectively. PVT1 knockdown significantly suppressed cell pyroptosis and downregulated the expression of inflammatory factors in LPS‑induced HK‑2 cells. The results also indicated that PVT1 served as a sponge of miR‑20a‑5p, and miR‑20a‑5p directly targeted NLRP3. miR‑20a‑5p knockdown significantly promoted LPS‑induced cell pyroptosis. Moreover, PVT1 knockdown inhibited LPS‑induced cell pyroptosis by targeting the miR‑20a‑5p/NLRP3 signalling pathway. The results of the present study suggested that PVT1 modulated NLRP3‑mediated pyroptosis in septic AKI by targeting miR‑20a‑5p, which might suggest significant potential therapeutic targets for septic AKI.

Mesenchymal stem cells (MSCs) have been reported to regulate the systemic inflammatory response and sepsis-induced immunologic injury pre-clinically. However, whether MSCs from different sources elicit identical effects remains to be elucidated. The present study compared the effect of bone marrow‑derived MSCs (BMSCs) and adipose tissue-derived MSCs (ADMSCs) in a murine model of lipopolysaccharide (LPS)‑induced sepsis. SPF BALB/c mice were induced with an injection of LPS (10 mg/kg; 1 mg/ml) via the tail vein. To compare the effect of MSCs on the septic mice, either saline, BMSCs or ADMSCs were injected via the tail vein 5 min following the administration of LPS. The survival rates and body temperatures of the mice were observed regularly up to 48 h. The serum levels of pro‑inflammatory cytokines, including tumour necrosis factor‑α, interleukin (IL)‑6 and IL‑8, anti‑inflammatory cytokines, including IL‑2, IL‑4 and IL‑10, and biochemical markers, including lactate, creatinine, alanine aminotransferase and aspertate aminotransferase, were analyzed at 6 h. The BMSCs and ADMSCs significantly reduced mortality rates, body‑temperature fluctuations, serum levels of biochemical markers and the majority of cytokines. However, the levels of IL‑8 in the BMSC and ADMSC groups were increased and decreased, respectively. These findings suggested that BMSCs and ADMSCs ameliorated sepsis-associated organ injury and mortality, and had a similar regulatory effect on pro‑ and anti‑inflammatory cytokines despite the different MSC sources. Therefore, BMSCs and ADMSCs may serve as novel treatment modalities for sepsis.

Ovarian cancer (OC) is the fifth leading cause of cancer‑associated mortality among women in developed countries. Numerous microRNAs are aberrantly expressed in epithelial (E) OC, and are involved in EOC formation and progression. As such, microRNAs may be investigated as diagnostic and prognostic molecular biomarkers, and therapeutic targets for patients with EOC. For instance, microRNA‑455 (miR‑455) is abnormally expressed in various types of human cancer. However, details on the expression level, biological roles and underlying mechanism of miR‑455 in EOC remain unclear. In the present study, the expression of miR‑455 in EOC was detected, and its association with clinical characteristics was analysed. The functional roles and underlying mechanisms of miR‑455 in EOC were also investigated. The results revealed that miR‑455 expression in EOC tissues and cell lines was significantly downregulated. Furthermore, miR‑455 downregulation was correlated with tumor size, International Federation of Gynecology and Obstetrics stage and lymph node metastasis of patients with EOC. Restoration of miR‑455 expression efficiently inhibited cell proliferation and invasion in vitro. Notch1 was identified as a direct target of miR‑455 in EOC. The mRNA and protein expression levels of Notch1 were higher in EOC tissues compared with in normal ovarian epithelial tissues. Spearman's correlation analysis indicated that miR‑455 expression was negatively correlated with the mRNA level of Notch1 in EOC tissues. Notch1 overexpression was able to restore the EOC cell proliferation and invasion abilities suppressed by miR‑455. The present study provided evidence that the dysregulation of the miR‑455/Notch1 signalling pathway may be essential for EOC occurrence and development. In addition, the results confirmed the tumor‑suppressive roles of miR‑455 in modulating EOC proliferation and invasion through regulation of Notch1 expression. Thus, miR‑455 may be a novel miRNA‑based therapeutic target to treat patients with EOC.

Stroke is a leading cause of cardiovascular morbidity, economic and social burden and mortality. Novel approaches are needed to address stroke prevention and treatment. The purpose of this study was to explore the effects of aloe polysaccharide on caspase-3 expression following cerebral ischemia reperfusion injury in rats. Male Wistar rats were randomly divided into 5 groups (16 rats in each group): aloe polysaccharide, ginkgo leaf tablet, nimodipine, model and sham surgery groups. The rats were administered the appropriate drug or normal saline for 7 days by gavage. A rat model of cerebral ischemia and reperfusion injury was established using the middle cerebral artery occlusion (MCAO) model. Caspase-3 protein and mRNA expression levels in the cerebral cortex were detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Results showed that caspase-3 protein and mRNA expression levels in the cerebral cortex in the aloe polysaccharide, ginkgo leaf tablet and nimodipine groups were significantly lower compared with the model group and were higher than the sham surgery group (P0.05). No significant difference was observed in caspase-3 protein and mRNA expression among the aloe polysaccharide, the ginkgo leaf tablet and the nimodipine groups (P0.05). In conclusion, aloe polysaccharide has a protective effect on cerebral ischemia that may be due to the inhibition of neuronal cell apoptosis.

Oculocutaneous albinism (OCA) is a group of heterogeneous and autosomal recessive disorders characterized by a reduction or complete loss of melanin biosynthesis in melanocytes. OCA type 1 (OCA1) is the most severe and common form of OCA, and is caused by mutations in the tyrosinase gene (TYR). The present study aimed to identify the genetic cause of OCA1 in a four‑generation consanguineous Chinese Han family. Complete physical examinations were performed and blood samples were collected from five members of the family and 100 unrelated healthy controls. Exome sequencing was conducted in the proband, followed by verification in other family members, using Sanger sequencing. Patients in the family presented with typical OCA1 features, including hypopigmentation of the skin and hair, and distinctive ocular changes. A homozygous missense variant, c.896G>A (p.R299H), in the TYR gene was identified in two patients, which co‑segregated with disease in the family. This variant was not present in the 100 healthy controls. These results expand the number of mutations identified to be responsible for OCA1 in the Chinese Han population, and may have implications for genetic counseling and clinical management of the disease.

Ibuprofen, a commonly administered nonsteroidal anti‑inflammatory therapeutic agent, is also a partial agonist of peroxisome proliferator‑activated receptor γ (PPARγ). The present study investigated the effects of ibuprofen on type 1 diabetic nephropathy (DN) in rats, and the potential mechanisms associated with the activation of PPARγ. Diabetic rats were induced through a single intraperitoneal injection of streptozotocin before oral treatment with ibuprofen or pioglitazone for 8 weeks. The 24‑h urine collection was performed for measurement of total protein content. The kidney was fixed in 10% formalin for periodic acid‑Schiff and Masson's trichrome staining. Blood and residual kidney tissue samples were collected to measure the associated biochemical parameters. Chronic ibuprofen treatment decreased urinary protein excretion, blood urea nitrogen, glomerular basement membrane thickening and renal fibrosis, which were accompanied by increases in PPARγ protein expression, glutathione (GSH) level, and superoxide dismutase (SOD) activity, decreases in cyclooxygenase 2 and inducible nitric oxide synthase protein expressions, as well as a decreased interleukin 1β (IL‑1β) level in the renal cortex of DN rats. Furthermore, the reduced IL‑1β level, increased GSH quantities and stronger SOD activity in the rat serum were evaluated in ibuprofen‑treated diabetic rats and were compared with untreated diabetic rats. Regarding GSH and IL‑1β levels, ibuprofen was identified to be superior to the positive control, pioglitazone, while levels of the other indices were identified to be similar. Thus, ibuprofen was observed to prevent the development of DN, caused by type 1 diabetes, by anti‑inflammatory and anti‑oxidative action, potentially via PPARγ activation.