Objective:To investigate the effects and mechanism of metformin on the wound healing of full-thickness skin defects in diabetic rats.Methods:This study was an experimental study. Eighteen 8-week-old male Sprague Dawley rats were divided into control group, diabetes group, and diabetes+metformin group according to complete random grouping method, with 6 rats in each group. The latter two groups of rats were used to create diabetic models, and then four circular full-thickness skin defect wounds with a diameter of 5 mm were made on the back of 18 rats. Metformin F-127 hydrogel was applied only to the wounds of rats in diabetes+metformin group. The wound healing status on post injury day (POD) 7 and 13 was observed and the wound healing rate was calculated. The wound tissue on POD 7 and 13 was collected for hematoxylin-eosin staining to measure the length of re-epithelialized epidermis and calculate the change rates in diameters of epidermal and dermal wounds, for immunohistochemical staining to detect the relative expressions of keratin 10 and proliferating cell nuclear antigen (PCNA), and for Western blotting to detect the protein expressions of keratin 10 and PCNA. The sample size in all the above experiments was 8 except that in the last experiment was 3. The correlations between the relative expressions of keratin 10 and PCNA in wound tissue in three groups of rats and their wound healing rates, and the correlation between the relative expressions of keratin 10 and PCNA in wound tissue were analyzed.Results:On POD 7, the wound healing rates of rats in diabetes group and diabetes+metformin group were 81.48% (77.89%, 85.53%) and 93.04% (92.51%, 94.24%), which were significantly lower than 100% (97.17%, 100%) in control group (with Z values of 2.37 and -3.36, respectively, P<0.05); the wound healing rate of rats in diabetes+metformin group was significantly higher than that in diabetes group ( Z=3.45, P<0.05). On POD 13, the wound healing rates of rats in control group and diabetes+metformin group were both 100% (100%, 100%), which were significantly higher than 94.47% (90.68%, 99.82%) in diabetes group (with Z values of 2.90 and -2.90, respectively, P<0.05). On POD 7, the change rates in epidermal wound diameter of rats in control group and diabetes+metformin group were significantly higher than that in diabetes group (with Z values of 3.36 and -2.74, respectively, P<0.05). The change rates in dermal wound diameter of rats in the three groups were similar on POD 7 and 13 ( P>0.05). The lengths of re-epithelialized epidermis of rats in control group and diabetes+metformin group on POD 13 were significantly longer than that in diabetes group (with Z values of 3.34 and -2.64, respectively, P<0.05). The relative expressions of keratin 10 in wound tissue of rats in diabetes group on POD 7 and 13 were significantly higher than those in control group (with Z values of -3.36 and -3.26, respectively, P<0.05) and diabetes+metformin group (with Z values of 3.36 and 3.15, respectively, P<0.05), and the relative expression of keratin 10 in wound tissue of rats in diabetes+metformin group on POD 7 was significantly lower than that in control group ( Z=3.05, P<0.05); the relative expressions of PCNA in wound tissue of rats in diabetes group on POD 7 and 13 were significantly lower than those in control group (with both Z values of 3.36, P<0.05) and diabetes+metformin group (with both Z values of -3.36, P<0.05). The protein expressions of keratin 10 in wound tissue of rats in control group and diabetes+metformin group on POD 7 as well as that in diabetes+metformin group on POD 13 were significantly lower than those in diabetes group ( P<0.05), and the protein expressions of PCNA in wound tissue of rats in control group and diabetes+metformin group on POD 7 were significantly higher than that in diabetes group ( P<0.05). There was a significant positive correlation between the relative expression of keratin 10 in wound tissue and the wound healing rate in control group and diabetes+metformin group of rats (with r values of 0.78 and 0.71, respectively, P<0.05), there was a significant negative correlation between the relative expression of PCNA in wound tissue and the wound healing rate in diabetes+metformin group of rats ( r=-0.60, P<0.05), and there was a significant negative correlation between the relative expressions of PCNA and keratin 10 in wound tissue of rats in diabetes group and diabetes+metformin group (with r values of -0.41 and -0.49, respectively, P<0.05). Conclusions:The diabetic rats with full-thickness skin defect wound exhibit delayed healing, accompanied by up-regulation of keratin 10 and down-regulation of PCNA in keratinocytes in the wound tissue. Metformin can promote wound healing in diabetic rats with full-thickness skin defects by down-regulating keratin 10 expression and up-regulating PCNA expression in keratinocytes in the wound tissue, and the wound healing rate was positively correlated with the expression of keratin 10 and negatively correlated with the expression of PCNA.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Toll-like receptor 3 (TLR3) is a member of the TLR family, mediating the transcriptional induction of type I interferons (IFNs), proinflammatory cytokines, and chemokines, thereby collectively establishing an antiviral host response. Studies have shown that unlike other TLR family members, TLR3 is the only RNA sensor that is utterly dependent on the Toll-interleukin-1 receptor (TIR)‍-domain-containing adaptor-inducing IFN-‍β (TRIF). However, the details of how the TLR3-TRIF signaling pathway works in an antiviral response and how it is regulated are unclear. In this review, we focus on recent advances in understanding the antiviral mechanism of the TRIF pathway and describe the essential characteristics of TLR3 and its antiviral effects. Advancing our understanding of TLR3 may contribute to disease diagnosis and could foster the development of novel treatments for viral diseases.

Bluetongue virus (BTV) causes Bluetongue (BT) of ruminants vectored by culicoides midges. It is also a classic model for studying the release mechanism of non-enveloped virus. This review begins with the infection and assembly of BTV, then summarizes the advances of different ways of releasing BTV. This includes BTV-induced autophagy and the release as extracellular vesicles via multivesicular bodies, BTV-induced apoptosis and the lytic release, as well as different pathways of release through budding via plasma membrane. The regulatory mechanisms of NS3 which is a key non-structural protein during the release of BTV are also discussed, providing a basis for further understanding the molecular mechanisms underpinning the infection, proliferation and release of BTV.
Animals ; Bluetongue ; Bluetongue virus ; Ceratopogonidae ; Sheep ; Viral Nonstructural Proteins

Objective: To investigate whether microRNA(miR)-214 can improve hyperglycemia induced pyroptosis in H9c2 cells through targeting caspase-1. Methods: H9c2 cells of rats those in good growth condition were selected and incubated into the T25 culture bottle after digestion and passage. Cells were cultured in an incubator at 37 ℃ with 5%CO₂, repeat passage was made after cell density reached about 80%, The 5^th to 8^th generations of cells were selected for the subsequent experiments. To observe the effect of overexpression of miR-214 on pyroptosis and caspase-1 expression in H9c2 cells induced by hyperglycemia, the cells were divided into 4 groups: Control group(H9c2 cells cultured normally), Hyperglycemia group (HG group, 50 mmol/L glucose was used to intervene H9c2 cells for 24 hours), miR-214 mimics+hyperglycosis group (mimics+HG group, H9c2 cells were transfected with miR-214 mimics for 24 hours and then treated with 50 mmol/L hyperglycosis for 24 hours), miR-214 mimic-negative control+hyperglycaemic group(MNC+HG group, H9c2 cells were transfected with miR-214 mimic-negative control for 24 hours and then treated with 50 mmol/L hyperglycaemic for 24 hours). In order to further verify the anti-pyroptosis effect of miR-214 was mediated by targeted inhibition on caspase-1, cells overexpressing caspase-1 were used in the rescue experiment. The cells overexpressing caspase-1 were divided into 4 groups: Hyperglycemia group (HG group, 50 mmol/L glucose was used to intervene H9c2 cells for 24 hours), miR-214 mimics+hyperglycosis group (mimics+HG group, H9c2 cells were transfected with miR-214 mimics for 24 hours and then treated with 50 mmol/L hyperglycosis for 24 hours), miR-214 mimics+hyperglycosis+recombinant adenovirus (Ad-caspase-1-EGFP) group with caspase-1 gene and EGFP green fluorescent protein expression (mimics+HG+Ad-caspase-1-EGFP group, H9c2 cells were transfected with caspase-1-green fluorescent protein-carrying adenovirus for 48 hours, followed by transfection of miR-214 mimics for 24 hours, and then treated with 50 mmol/L hyperglycaemia for 24 hours), miR-214 mimics+HG+Ad-EGFP empty virus group (mimics+HG+Ad-EGFP group, H9c2 cells were transfected with empty adenovirus containing green fluorescent protein for 48 hours, followed by transfection with miR-214 mimics for 24 hours, and then treated with 50 mmol/L hyperglycosis for 24 hours). The mRNA expression levels of miRNA-214 and caspase-1 in cells were detected by real-time quantitative PCR. The expression and localization of caspase-1 protein were detected by immunofluorescence assay. Western blot was used to detect protein expression levels of procaspase-1, cleaved caspase-1, NLRP3 and ACS with β-actin as internal reference. The secretion of IL-1β and IL-18 in cell culture medium was detected by ELISA. The correlation between miR-214 and caspase-1 was detected by double luciferase reporter gene. Results: (1) The mRNA expression levels of miR-214 and caspase-1 in each group: the mRNA expressions of miR-214 in HG group and MNC+HG group were significantly lower than that in control group(P<0.05). The mRNA expression of miR-214 in mimics+HG group was significantly higher than that in control group (P<0.05). The mRNA expression levels of caspase-1 in HG group and MNC+HG group were significantly higher than that in control group(P<0.05). The mRNA expression level of caspase-1 in mimics+HG group was lower than that in control group(P<0.05). (2) The expression of caspase-1 in each group: the green fluorescence intensity in the control group was weak, which was strong in the HG group and MNC+HG group. The green fluorescence expression was weaker in mimics+HG group than in HG group. (3) ASC and NLRP3 protein expression levels in each group: ASC and NLRP3 protein expression levels in HG group and MNC+HG group were higher than those in control group(P<0.05). ASC and NLRP3 protein expression levels were significantly lower in mimics+HG group than in mimics+HG group (P<0.05). (4) The secretion of IL-1β and IL-18 in the cell culture medium of each group: the content of IL-1β and IL-18 in the cell culture medium of HG group and MNC+HG group was significantly higher than that of control group (P<0.05). The content of IL-1β and IL-18 in the cell culture medium of mimics+HG group was significantly lower than that of the HG group (P<0.05). (5) Correlation between miR-214 and caspase-1: miR-214 specifically binds to caspase-1 3 ′UTR. Meanwhile, Western blot results showed that cleaved caspase-1 protein expression levels were significantly higher in both HG group and MNC+HG group than in control group (P<0.05). The levels of cleaved caspase-1 were significantly lower in mimics+HG group than in HG group (P<0.05). There was no significant difference in procaspase-1 expression among groups (P>0.05). (6) The expression levels of procaspase-1, cleaved caspase-1, ASC and NLRP3 in each group in rescue experiment: there was no significant difference in the expression of procaspase-1 in each group (P>0.05). Cleaved caspase-1, ASC and NLRP3 protein expressions were significantly lower in mimics+HG group than in HG group (P<0.05). However, cleaved caspase-1, ASC and NLRP3 protein expressions were significantly higher in mimics+HG+ Ad-caspase-1-EGFP group than in mimics+HG group (P<0.05). (7) The expression of IL-1β and IL-18 in rescue experiment: the secretions of IL-1β and IL-18 in the cell culture medium of the mimics+HG group were significantly lower than that of HG group (P<0.05), which were significantly higher in mimics+HG+Ad-caspase-1-EGFP group than in mimics+HG group (P<0.05). Conclusion miR-214 can improve the hyperglycemia induced pyroptosis in H9c2 cells by targeted inhibition of the caspase-1.

Objective To investigate whether microRNA(miR)?214 can improve hyperglycemia induced pyroptosis in H9c2 cells through targeting caspase?1. Methods H9c2 cells of rats those in good growth condition were selected and incubated into the T25 culture bottle after digestion and passage. Cells were cultured in an incubator at 37℃with 5%CO2, repeat passage was made after cell density reached about 80%, The 5th to 8th generations of cells were selected for the subsequent experiments. To observe the effect of overexpression of miR?214 on pyroptosis and caspase?1 expression in H9c2 cells induced by hyperglycemia, the cells were divided into 4 groups: Control group(H9c2 cells cultured normally), Hyperglycemia group (HG group, 50 mmol/L glucose was used to intervene H9c2 cells for 24 hours), miR?214 mimics+hyperglycosis group (mimics+HG group, H9c2 cells were transfected with miR?214 mimics for 24 hours and then treated with 50 mmol/L hyperglycosis for 24 hours), miR?214 mimic?negative control+hyperglycaemic group(MNC+HG group, H9c2 cells were transfected with miR?214 mimic?negative control for 24 hours and then treated with 50 mmol/L hyperglycaemic for 24 hours). In order to further verify the anti?pyroptosis effect of miR?214 was mediated by targeted inhibition on caspase?1, cells overexpressing caspase?1 were used in the rescue experiment. The cells overexpressing caspase?1 were divided into 4 groups: Hyperglycemia group (HG group, 50 mmol/L glucose was used to intervene H9c2 cells for 24 hours), miR?214 mimics+hyperglycosis group (mimics+HG group, H9c2 cells were transfected with miR?214 mimics for 24 hours and then treated with 50 mmol/L hyperglycosis for 24 hours), miR?214 mimics+hyperglycosis+recombinant adenovirus (Ad?caspase?1?EGFP) group with caspase?1 gene and EGFP green fluorescent protein expression (mimics+HG + Ad?caspase?1?EGFP group, H9c2 cells were transfected with caspase?1?green fluorescent protein?carrying adenovirus for 48 hours, followed by transfection of miR?214 mimics for 24 hours, and then treated with 50 mmol/L hyperglycaemia for 24 hours), miR?214 mimics+HG+Ad?EGFP empty virus group (mimics+HG+Ad?EGFP group, H9c2 cells were transfected with empty adenovirus containing green fluorescent protein for 48 hours, followed by transfection with miR?214 mimics for 24 hours, and then treated with 50 mmol/L hyperglycosis for 24 hours). The mRNA expression levels of miRNA?214 and caspase?1 in cells were detected by real?time quantitative PCR. The expression and localization of caspase?1 protein were detected by immunofluorescence assay. Western blot was used to detect protein expression levels of procaspase?1, cleaved caspase?1, NLRP3 and ACS with β?actin as internal reference. The secretion of IL?1β and IL?18 in cell culture medium was detected by ELISA. The correlation between miR?214 and caspase?1 was detected by double luciferase reporter gene. Results (1) The mRNA expression levels of miR?214 and caspase?1 in each group: the mRNA expressions of miR?214 in HG group and MNC+HG group were significantly lower than that in control group(P<0.05). The mRNA expression of miR?214 in mimics+HG group was significantly higher than that in control group (P<0.05). The mRNA expression levels of caspase?1 in HG group and MNC+HG group were significantly higher than that in control group(P<0.05). The mRNA expression level of caspase?1 in mimics+HG group was lower than that in control group(P<0.05). (2) The expression of caspase?1 in each group: the green fluorescence intensity in the control group was weak, which was strong in the HG group and MNC+HG group. The green fluorescence expression was weaker in mimics+HG group than in HG group. (3) ASC and NLRP3 protein expression levels in each group: ASC and NLRP3 protein expression levels in HG group and MNC+HG group were higher than those in control group(P<0.05). ASC and NLRP3 protein expression levels were significantly lower in mimics+HG group than in mimics+HG group (P<0.05). (4) The secretion of IL?1β and IL?18 in the cell culture medium of each group: the content of IL?1β and IL?18 in the cell culture medium of HG group and MNC+HG group was significantly higher than that of control group (P<0.05). The content of IL?1β and IL?18 in the cell culture medium of mimics+HG group was significantly lower than that of the HG group (P<0.05). (5) Correlation between miR?214 and caspase?1: miR?214 specifically binds to caspase?1 3 ＇UTR. Meanwhile, Western blot results showed that cleaved caspase?1 protein expression levels were significantly higher in both HG group and MNC+HG group than in control group (P<0.05). The levels of cleaved caspase?1 were significantly lower in mimics+HG group than in HG group (P<0.05). There was no significant difference in procaspase?1 expression among groups (P>0.05). (6) The expression levels of procaspase?1, cleaved caspase?1, ASC and NLRP3 in each group in rescue experiment: there was no significant difference in the expression of procaspase?1 in each group (P>0.05). Cleaved caspase?1 , ASC and NLRP3 protein expressions were significantly lower in mimics+HG group than in HG group (P<0.05). However, cleaved caspase?1, ASC and NLRP3 protein expressions were significantly higher in mimics+HG+Ad?caspase?1?EGFP group than in mimics+HG group (P<0.05). (7) The expression of IL?1β and IL?18 in rescue experiment: the secretions of IL?1β and IL?18 in the cell culture medium of the mimics+HG group were significantly lower than that of HG group (P<0.05), which were significantly higher in mimics+HG+Ad?caspase?1?EGFP group than in mimics+HG group (P<0.05). Conclusion miR?214 can improve the hyperglycemia induced pyroptosis in H9c2 cells by targeted inhibition of the caspase?1.

Objective To investigate the clinical and prognostic significance of ABO promotor methylation level in adult patients with leukemia and myelodydysplastic syndrome(MDS). Methods ABO promoter methylation level of 182 malignant hematological disease patients and 68 normal controls were detected by bisulfite sequencing PCR. Then clinical features and outcome were compared between hypermethylation group and hypomethylation group. Results The median methylation rate of ABO promoter in newly diagnosed acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) were 46.98％ and 11.01％ respectively, which were both higher than that in controls (2.30％, P<0.05). The methylation rates in remission AML and ALL were 1.58％and 2.30％respectively, which were comparable with that in normal group (P>0.05). As to relapse AML and ALL, methylation rates were 41.26％ and 17.50％respectively, also significantly higher than that in controls (P<0.05).In patients with chronic myeloid leukemia (CML) chronic phase, the median methylation rate was 1.00％, which was similar to normal group. But a CML patient who transformed to ALL hadextremely high methylation rate 92.56％. The median methylation rate in patients with MDS significantly elevated as 5.81％ compared with that in controls (P<0.05). The median overall survival (OS) of ALL and AML (non-M3) patients with hypermethylation were 12.5 months and 15.3 months, which were significantly shorter than those with hypomethylation (24.0 months and 20.0 months) (P<0.05). The median disease-free survival (DFS) of ALL and AML (non-M3) patients with hypermethylation were 9.9 months and 12.0 months, which were significantly shorter than those with hypomethylation (22.3 months and 18.5 months), (P<0.05). Multivariable analysis suggested that ABO promoter methylation level was an independent predictive factor of OS and DFS in ALL and AML (non-M3) patients. Conclusion ABO promoter hypermethylation is closely related to genesis, development and prognosis of leukemia and MDS. Hypermethylationis related to a clinical poor prognosis compare with hypomethylation.

Objective To evaluate effects of targeted silencing of growth arrest and DNA damage inducible gene 45α (Gadd45α) by small interference RNA (siRNA) on the invasion and migration of a cutaneous squamous cell carcinoma cell line A431.Methods Real-time fluorescence-based quantitative PCR and Western blot analysis were performed to detect the mRNA and protein expression of A431 and Colon16 cells respectively,and then A431 cells with highly expressed Gadd45α served as a research object.Cultured A431 cells were divided into 3 groups:experimental group transfected with Gadd45α-siRNA-1,negative control group transfected with negative control siRNA,and blank control group receiving no treatment.After the RNA interference,the mRNA and protein expression of Gadd45α in the above 3 groups were measured by real-time fluorescence-based quantitative PCR and Western blot analysis,respectively,and the effect of the RNA interference on the invasion and migration abilities of A431 cells was evaluated by Transwell and wound scratch assays.Results Gadd45α mRNA and protein were highly expressed in the A431 cells.After the RNA interference,the experimental group showed markedly lower mRNA and protein expressions of Gadd45 in the A431 cells (0.286 ± 0.013,0.33 ± 0.007,respectively) compared with the negative control group (1.028 ± 0.183,0.87 ± 0.002,respectively)and blank control group (1.001 ± 0.057,0.86 ± 0.004,respectively),and there were significant differences in the mRNA and protein expressions of Gadd45 among the 3 groups (F =5 893.857,2 763.000,both P ＜ 0.001).The number of A431 cells crossing the polycarbonate membrane was higher in the experimental group (66.33 ± 3.79) than in the negative control group (26.00 ± 4.36) and the blank control group (28.33 ± 4.16),and there was a significant difference among the 3 groups (F =20.084,P =0.002).Moreover,the wound scratch assay showed that the number of migrating A431 cells per high-power field was significantly higher in the experimental group than in the negative control group and the blank control group (315.33 ± 6.66,154.67 ± 2.08,130.67 ± 3.51 respectively;F =1 676.255,P ＜ 0.001).Conclusion Gadd45α is highly expressed in the cutaneous squamous cell carcinoma cell line A431,and targeted silencing of Gadd45α gene can enhance the in vitro invasion and migration abilities of A431 cells.

Objective: To explored the effect and related mechanism of miRNA-21 on hydrogen peroxide-induced C-kit⁺ cardiac stem cells apoptosis. Methods: C-kit⁺ cardiac stem cells were isolated from SD rats by the methods of enzyme digestion and magnetic bead. Cells were divided into the following experimental groups: (1) negative control mimics (NCM)group: cells were transfected with negative control miRNA-21 mimics for 48 hours; (2)mimics group: cells were transfected with miRNA-21 mimics for 48 hours; (3) NCM+ H₂O₂ group: negative control miRNA-21 mimics were transfected into cells for 48 hours and then treated with 100 μmol H₂O₂ for 2 hours; (4)mimics+ H₂O₂ group: miRNA-21 mimics were transfected into cells for 48 hours and then treated with 100 μmol H₂O₂ for 2 hours. mRNA of miRNA-21 was detected by RT-PCR. The apoptosis rate of C-kit⁺ cardiac stem cells was determined using the annexin V-FITC/PI staining assay. Western blot was employed to measure the expression of apoptosis related proteins(Caspase-3, Bax, and Bcl-2). Results: (1) Compared with the NCM group, the mRNA expression level of miRNA-21 was significantly up-regulated in mimics group, while obviously down-regulated in NCM+ H₂O₂ group(all P<0.05). Compared with the mimics group, the mRNA expression levels of miRNA-21 in mimics+ H₂O₂ group was significantly downregulated (P<0.05), but remarkably upregulated compared with the NCM+ H₂O₂ group(P<0.05). (2) Flow cytometry results indicated that the early apoptosis rates were similar between the NCM group and mimics group ((4.57±3.45)% vs. (5.13±3.21)%, P>0.05). Compared with the NCM group, the early apoptosis rates were remarkably increased ((79.07±5.75)% vs.(4.57±3.45)%, P<0.05) in NCM+ H₂O₂ group. Compared with the mimics group, the early apoptosis was significantly up-regulated in the mimics+ H₂O₂ group ((30.27±1.36)% vs.(5.13±3.21)%, P<0.05), which were further down-regulated in mimics+ H₂O₂ group compared with the NCM+ H₂O₂ group ((30.27±1.36)% vs.(79.07±5.75)%, P<0.05). (3) Western blot results showed similar protein expression of Caspase-3, Bax and Bcl-2 between NCM group and mimics group(all P>0.05). Compared with the NCM group, the Caspase-3 and Bax protein expression was significantly increased in NCM+ H₂O₂ group (all P<0.05), but the protein expression level of Bcl-2 was similar between the 2 groups(P>0.05). The Caspase-3 and Bax protein expression was markedly decreased, while Bcl-2 apparently increased in the mimics+ H₂O₂ group compared with the NCM+ H₂O₂ group(all P<0.05). Conclusion Overexpression of miRNA-21 protects the C-kit⁺ cardiac stem cells from apoptosis caused by oxidative stress through downregulating proapoptotic and upregulating the antiapoptotic proteins.

OBJECTIVE:To observe clinical efficacy and safety of individual antiviral therapy of tenofovir combined with inter-feron α1b for chronic hepatitis B (CHB). METHODS:96 CHB patients were randomly divided into control group,observation group A and observation group B,with 32 cases in each group. Control group was given entecavir orally,0.5 mg,qd;observation group A was given tenofovir orally,1 piece,qd;observation group B was additionally given interferon α1b,50 μg,3 times a week,on the basis of observation group A. The treatment course lasted for 48 weeks in 3 groups. Clinical efficacy of 3 groups was compared,and the changes of serum liver function indexes,HBV-DNA negative conversion rate and the occurrence of ADR were compared before and after treatment. RESULTS:The total effective rate of observation group B(84.38%)was significantly higher than that of observation group A(62.60%)and control group(37.50%),and that of observation group A was significantly higher than control group,with statistical significance (P<0.05). Compared with before treatment,the serum levels of AST,ALT and TBIL were significantly decreased after treatment in 3 groups;the observation group B were significantly lower than those of obser-vation group A and control group,with statistical significance(P<0.05);there was no statistical significance between observation group A and control group(P>0.05). The negative rate of HBV-DNA in observation group B were significantly higher than those in control group and observation group A after 12 and 24 weeks of treatment,with statistical significance(P<0.05);there was no statistical significance between observation group A and control group (P>0.05). No obvious ADR was found in 3 groups. CON-CLUSIONS:Tenofovir combined with interferon α1b shows significant clinical efficacy for CHB,and is significantly better than that of entecavir and tenofovir alone.