ABSTRACT
Objective:To investigate the repair effect of amphiregulin (Areg) on injured lung tissue in mice with acute respiratory distress syndrome (ARDS) and its underlying mechanism.Methods:The ARDS mouse model was made by tracheal infusion of lipopolysaccharide (LPS), and bronchoalveolar lavage fluid (BALF) was extracted for 7 consecutive days. Adult male C57BL/6 mice were randomly (random number) divided into 5 groups ( n=4 per group): (1) Control group; (2) Areg group: mice were treated intraperitoneally (i.p.) with recombinant Areg; (3) LPS+PBS group; (4) LPS+Areg group; and (5) LPS+Anti-Areg group; mice were instilled with LPS, then were injected i.p. with PBS, Areg or Areg neutralization antibody (Anti-Areg) 30 min later. Lung tissue and BALF were extracted at day 1, 3, 5 and 7 after ARDS. HE staining was used to evaluate the pathological changes of lung tissues. The total protein content in BALF was detected by BCA method, and the concentrations of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β and immunoglobulin M (IgM) were determined by ELISA method. The phosphorylated levels of epidermal growth factor receptor (EGFR) and expressions of proliferating cell nuclear antigen (PCNA) and surface proteins-C (SP-C) were tested by Western blot. The immunofluorescence was used to detect the co-expression of PCNA and SP-C in lung tissues. One-way analysis of variance was used to compare the mean values of normally distributed measurement data between groups. Comparisons between groups were performed using the least significant difference t-test. Results:Compared with that at before modeling [(51.05±2.47) pg/mL], Areg concentrations were increased significantly at day 1 [(71.97±6.51) pg/mL; P<0.01] and day 3 [(147.58±7.56) pg/mL, P<0.01] in the BALF after ARDS. At day 1 after ARDS, there were significant interstitial edema, neutrophil infiltration and alveolar collapse in the LPS+PBS group and LPS+Areg group. Compared with the LPS+PBS group at day 3, 5 and 7, the pathological changes of lung tissues were notably improved in the LPS+Areg group, while were more serious in the LPS+Anti-Areg group. Compared with the control group, the LPS+PBS group had higher levels of neutrophil number, total protein, IgM, TNF-α, IL-1β, and IL-6. However, Areg treatment significantly reduced the levels of these indicators. Moreover, the expressions of PCNA (1.34±0.10), SP-C (1.48±0.10) and p-EGFR (0.92±0.032) in the LPS+Areg group were significantly up-regulated compared with those in the LPS+PBS group (0.88±0.03, 1.06±0.15, and 0.68±0.03, all P<0.01). And compared with the LPS+PBS group, PCNA and SP-C double positive cells were significantly increased in the LPS+Areg group, but decreased in the LPS+Anti-Areg group. Conclusions:Areg enhances the proliferation of alveolar typeⅡ epithelial cells by activating EGFR pathway, therefore promotes the repair of lung tissues during ARDS development.
ABSTRACT
AIM: To observe the effect and possible mechanism of stimulation of Yes-associated protein (YAP) activity on acute lung injury and repair induced by LPS in mice. METHODS: Ninety adult male ICR mice were divided into two groups: acute lung injury model group induced by LPS (7.5 mg/kg, i.p.) and LPS+XMU treatment (1 mg•kg-1•d-1) group. At 0 h, 24 h, 48 h and 72 h after LPS injection, the contents of TNF-α and IL-6 in bronchoalveolar lavage fluid (BALF) were detected by ELISA method. The activity of myeloperoxidase (MPO) and the content of protein in BALF were evaluated by chemical technique. The protein level of nuclear YAP, cytosol phosphorylated YAP (P-YAP), connective tissue growth factor (CTGF) and proliferating cell nuclear antigen (PCNA) in lung were analyzed by Western blot. RESULTS:The protein level of nuclear YAP at 24 h, 48 h and 72 h in lung of LPS+XMU group were up-regulated than those of LPS group by 39.2%, 148.1% and 42.9%, and the protein level of CTGF in lung were up-regulated than those of LPS group by 186.6%, 10.1% and 146.1% (P<0.05), respectively, while the protein level of cytosol P-YAP was down-regulated. The content of IL-6 and TNF-α at 24 h in BALF of LPS+XMU group were lower than those of LPS group by 28.4% and 23.7%, and the activity of MPO and the content of TNF-α at 48 h in BALF were lower by 13.5% and 39.5%, and the content of IL-6 and TNF-α at 72 h in BALF were lower by 42.8% and 16.7% (P<0.05), respectively. The protein level of PCNA at 48 h and 72 h in lung of LPS+XMU group were up-regulated than those of LPS group by 44.2% and 14.9% (P<0.05), respectively, while there was no significant difference at 24 h. The content of protein at 24 h, 48 h and 72 h in BALF of LPS+XMU group were lower than those of LPS group by 32.4%, 46.0% and 26.3% (P<0.05), respectively. The pathological changes showed a significantly attenuated tissue injury and accelerated recovery from lung injury in LPS+XMU group compared with mice injected with LPS alone at each times point. CONCLUSION: Stimulation of YAP activity attenuates lung injury and promotes lung recovery by alleviating lung inflammation and injury at injury phase, but by promoting inflammation resolution and stimulating cell proliferation at repair phase.
ABSTRACT
Objective: To study the effect of Matrilin-4 on the reparative dentin formation in the rats after dental pulp injury, and to explore its possibility to be used as a new capping agent. Methods: A total of 28 male Wistar rats were selected. A cavity on the occlusal surface of maxillary first molars on both sides was prepared in each rat. Matrilin-4 was applied on the left exposed pulp (Matrilin-4 group), and PBS was applied on the right exposed pulp (PBS group); and the cavities in both sides were covered with glass ions. On days 3, 7, 14 and 28 after operation, the rats were sacrificed, and the maxillary first molars on both sides of the rats were selected. HE staining and immunohistochemistry staining were used to observe and analyze the reparative dentin formation and the expression of dentin sialoprotein (DSP) in the odontoblasts. Results: The HE staining results showed that there were less inflammatory cells under the exposed pulp in that Matrilin-4 group at 3 d after operation compared with PBS group, and obvious vasodilation was found. At 7 d after operation, the inflammatory reaction under the exposed pulps in two groups was aggravated, but the inflammatory reaction in Matrilin-4 group was significantly lighter than that in PBS group, and the prophase dentin formation was found. After injury of 14 d, the pulp-exposed areas were covered by more complete dentin bridge in Matrilin-4 group; at 28 d after operation, compared with PBS group, there was a thick, complete and reparative dentin bridge under the exposed pulps, composed of tubular dentin in Matrilin-4 group, and there were reorganized odontoblastic layers beneath the dentin bridge. The results of immunohistochemistry showed that the positive expression strengths of DSP in the odontoblasts of the rats in two groups were gradually increased at 3, 7 and 14 d after operation, and were decreased at 28 d. The positive expression strengths of DSP in the odontoblast of the rats in Matrilin-4 group were stronger than those in PBS group at each time point after operation, and the positive expression strength reached the peak at 14 d. Conclusion: Compared with PBS group, the positive expression strength of DSP in the odontoblasts of the rats in Matrilin-4 group had significant differences (P<0.01) at 3, 7 and 14 d.
ABSTRACT
The mammalian central nervous system (CNS) is considered an immune privileged system as it is separated from the periphery by the blood brain barrier (BBB). Yet, immune functions have been postulated to heavily influence the functional state of the CNS, especially after injury or during neurodegeneration. There is controversy regarding whether adaptive immune responses are beneficial or detrimental to CNS injury repair. In this study, we utilized immunocompromised SCID mice and subjected them to spinal cord injury (SCI). We analyzed motor function, electrophysiology, histochemistry, and performed unbiased RNA-sequencing. SCID mice displayed improved CNS functional recovery compared to WT mice after SCI. Weighted gene-coexpression network analysis (WGCNA) of spinal cord transcriptomes revealed that SCID mice had reduced expression of immune function-related genes and heightened expression of neural transmission-related genes after SCI, which was confirmed by immunohistochemical analysis and was consistent with better functional recovery. Transcriptomic analyses also indicated heightened expression of neurotransmission-related genes before injury in SCID mice, suggesting that a steady state of immune-deficiency potentially led to CNS hyper-connectivity. Consequently, SCID mice without injury demonstrated worse performance in Morris water maze test. Taken together, not only reduced inflammation after injury but also dampened steady-state immune function without injury heightened the neurotransmission program, resulting in better or worse behavioral outcomes respectively. This study revealed the intricate relationship between immune and nervous systems, raising the possibility for therapeutic manipulation of neural function via immune modulation.
ABSTRACT
Objective To investigate the effects of Hippo signaling pathway on lung injury repair of mesenchymal stem cells (MSC) in acute respiratory distress syndrome (ARDS) and its mechanism. Methods Mouse bone marrow-derived MSC (mMSCs) cell lines with low expression of large tumor suppressor 2 (LATS2) were constructed by lentiviral vector transfection. Male C57BL/6 mice aging 6-8 weeks old were divided into four groups according to random number table (n = 36). The ARDS animal model (ARDS group) was reproduced by intratracheally injection of 2 g/L lipopolysaccharide (LPS) 50 μL, the normal saline (NS) control group was injected with an equal volume of NS. After 4 hours of model reproduction, 5×104 mMSCs transfected with blank lentivirus vector (MSC-shcontrol group) or shLATS2 lentivirus vector (MSC-shLATS2 group) were transplanted intratracheally, while NS control group and ARDS group were injected with equal volume of phosphate buffered saline (PBS). Mice were sacrificed at 3, 7, and 14 days after modeling, and lung tissue and bronchoalveolar lavage fluid (BALF) were harvested. Near-infrared fluorescence imaging, immunofluorescence staining and Western Blot were used to track mMSCs in lung tissue. Retension and proportion of mMSC differentiation into type Ⅱ alveolar epithelial cells (AECⅡ) were evaluated. Lung tissue wet weight/body weight ratio (LWW/BW) and total protein (TP) and albumin (ALB) in BALF were determined to reflect pulmonary edema. The expression of Occludin protein in lung epithelium was tested by Western Blot to reflect permeability of epithelium. The levels of interleukins (IL-1β, IL-6, IL-10) in BALF were assessed by enzyme-linked immunosorbent assay (ELISA) to reflect lung inflammation. Hematoxylin-eosin (HE) staining and modified Masson staining were carried out, and the scores were assessed to reflect lung injury and evaluate pulmonary fibrosis. Results The signal intensity of isolated lung fluorescence images at 3 days in the MSC-shLATS2 group was significantly higher than that in the MSC-shcontrol group (fluorescence intensity: 0.039±0.005 vs. 0.017±0.002, P < 0.05), the number of green fluorescent protein (GFP)-positive cells in lung tissue was also significantly higher than that in the MSC-shcontrol group (cells/HP:29.65±6.98 vs. 17.50±4.58, P < 0.05), but they all decreased with time; and the proportion of mMSCs differentiated into AECⅡ was significantly increased [(64.12±15.29)% vs. (19.64±3.71)%, P < 0.05]. Compared with the NS control group, the levels of surface active protein C (SPC) and Occludin protein in the ARDS group were significantly decreased, LWW/BW ratio and TP, ALB and inflammatory factors levels in BALF were significantly increased; extensive alveolar and interstitial edema, hemorrhage and diffuse inflammatory cell infiltration were found in lung tissue, and the lung injury score was significantly increased; collagen fibers were deposited in alveolar septum and alveolar cavity, and pulmonary fibrosis score was also increased significantly. Compared with the ARDS group, the expression levels of SPC and Occludin at 14 days in the MSC-shcontrol group and the MSC-shLATS2 group were significantly increased (SPC/β-actin: 0.51±0.12, 0.68±0.10 vs. 0.27±0.08, Occludin/β-actin: 0.49±0.19, 0.79±0.11 vs. 0.25±0.08, all P < 0.05), TP, ALB, IL-1β, IL-6 levels in BALF at 3 days were significantly decreased [TP (g/L): 8.08±1.72, 5.12±0.87 vs. 12.55±2.09; ALB (g/L): 0.71±0.21, 0.44±0.18 vs. 1.18±0.29, IL-1β(ng/L): 99.26±14.32, 60.11±8.58 vs. 161.86±25.17, IL-6 (ng/L): 145.54±13.29, 101.74±11.55 vs. 258.79±27.88, all P < 0.05], and IL-10 was significantly increased (ng/L: 190.83±22.61, 316.65±37.88, both P < 0.05). Furthermore, all the above parameters in the MSC-shLATS2 group were significantly improved as compared with those in the MSC-shcontrol group (all P < 0.05). LWW/BW ratio in the MSC-shLATS2 group was significantly lower than that in the ARDS group and the MSC-shcontrol group (mg/g: 9.85±1.51 vs. 16.78±1.92, 14.88±1.74, both P < 0.05). Conclusion Inhibiting Hippo signaling pathway by low expression of LATS2 could promote the retention of mMSCs in lung tissue and differentiation into AECⅡcells of ARDS mice, improve pulmonary edema and alveolar epithelial permeability, regulate pulmonary inflammatory response, and alleviate pathological damage and fibrosis of lung tissue.
ABSTRACT
Objectives To determine the effect of Hippo signaling pathway on lung injury repair of bone-marrow derived mesenchymal stem cells (mMSCs) in murine lipopolysaccharide (LPS) induced acute respiratory distress syndrome (ARDS).Methods C57BL/6 mouse bone marrow-derived MSC (mMSCs) cell lines with low expression of large tumor suppressor 1 (LATS 1) were constructed by lentiviral vector transfection.ARDS was modeled by intratracheally injection of 2 mg/mL lipopolysaccharide (LPS)50 μL.C57BL/6 mice were randomly(random number) divided into four groups (n=36):normal control group,ARDS group,ARDS mice transplanted with mMSCs transfected with blank lentivirus vector (MSC-shcontrol group) or sh-LATS 1 lentivirus vector (MSC-shLATS 1 group).Mice were sacrificed at 3,7,and 14 d after modeling,and lung tissue and bronchoalveolar lavage fluid (BALF) were collected.Near-infrared fluorescence imaging,immunofluorescence staining and Western blot were used to evaluate retention and differentiation of mMSCs in lung tissue.Lung tissue wet weight/body weight ratio (LWW/BW) and total protein (TP) and albumin (ALB) in BALF were determined to reflect pulmonary edema.The expression of Occludin protein in lung epithelium was tested by Western blot.The levels of interleukins (IL-1β,IL-6,and IL-10) in BALF were assessed by enzyme-linked immunosorbent assay (ELISA).Lung injury score and pulmonary fibrosis score in lung tissue were assessed.Results The retention ofmMSCs at 3,7 and 14 d in the MSC-shLATS1 group were significantly higher than those in the MSC-shcontrol group [(26.25±4.58) vs (12.13±3.75) cells/HP,(20.49±3.86) vs (9.97±2.76) cells/HP,and (13.77±3.55) vs (6.89±2.10) cells/HP.all P＜0.05],so was the differentiation of mMSCs into type Ⅱ alveolar epithelial cells at 14 d [(64.12±15.29)％ vs (19.64±3.71)％,P＜0.05].LWW/BW and TP and ALB in BALF at 3 and 14 d in the MSC-shLATS1 group [(9.85±1.51),(6.11±0.83) (mg/g) and (5.12±0.87),(3.05±0.87) (mg/mL)and (0.44±0.18),(0.33±0.04) (mg/mL)] were higher than those in the MSC-shcontrol group [(14.88± 1.74),(8.04±l.70)(mg/g) and (8.08±1.72),(5.94±1.20) (mg/mL) and (0.71±0.21),(1.07±0.29) (mg/mL)] (all P＜0.05),so was the relative expression of Occludin protein[(0.79±0.11) vs (0.49±0).19),(P＜0.05)].The levels of IL-1β and IL-6(pg/mL) in BALF in the MSC-shLATS1 group [(60.11±8.58),(101.74±11.55)] was lower than those in the MSC-shcontrol group [(99.26±14.32),(145.54±13.29)] (all P＜0.05),but the levels of IL-10 in BALF in the MSC-shLATS 1 group (316.65±37.88)pg/mL was higher than those in the MSC-shcontrol group (190.83±22.61)pg/mL (P＜0.05).Lung injury scores at 3 and 14 d in the MSC-shLATS1 group [(7.18±1.12),(3.33±0.49)] was lower than those in the MSC-shcontrol group [(9.72±1.45),(5.11±0.86)] (all P＜0.05),so was pulmonary fibrosis score at 14 d [(0.68±0.12) vs (1.47±0.18),P＜0.05].Conclusion Inhibition of Hippo signaling pathway through underexpression of LATS1 could improve the therapeutic effects of mMSCs in murine LPS-induced ARDS.
ABSTRACT
Bone marrow mesenchymal stem cells (BMSCs) are a class of cells that can differentiate into different kind of corneal cells both in vitro and in vivo,which include corneal epithelial cells,limbal epithelial cells and corneal stromal cells.BMSCs could differentiate into corneal epithelial cells after transplantation,which can not only repair the damaged corneal,but also relieve inflammatory injury caused by the inflammatory cell infiltration.The other function of BMSC transplantation is to reduce the rejection after corneal transplantation by inhibiting cell damage and apoptosis.BMSC can also express a variety of factors on the carrier,these factors paly the important role in promoting the proliferation of limbal stem cells.These findings above provide a new direction for the fundamental study of ophthalmology,and put forward new clinical treatment ideas for corneal disease,both of them have broad protect for development,in this paper,the research status and progress of BMSC in the repair of corneal injury are reviewed.
ABSTRACT
Objective To observe the early effect of Fructus mume extract on KIM-1 and OPN levels in rats with kidney stone formation induced by nanobacteria and to investigate the therapeutic significance of F.mume extract on early kidney stone formation.Methods Nanobacteria were separated and cultured from human upper urinary calculi.The study group appropriately included 54 healthy male SD rats.The renal calculus model was constructed by tail vein injection of nanobacteria.A kidney stone model was created with an F.mume extract intervention,and rats were killed at different stages of the intervention.Real-time polymerase chain reaction was used to detect the KIM-1 mRNA expression in rat renal tissue,and the KIM-1 concentration in urine was detected by using enzyme-linked immunosorbent assay.We detected kidney tissue stone crystals and OPN expression by using hematoxylin-eosin staining and immunohistochemistry.Results Renal tubules of the experimental model were significantly expanded,that is,the formation of renal tubular stones.The early KIM-1 and OPN expression levels were increased.The above-mentioned changes positively correlated with the injection time of the nanobacteria,and F.mume extract antagonized the changes.Conclusion F.mume extract may be useful for the repair of renal injury to reduce kidney stone formation,which may be related to the gene regulation of KIM-1 and OPN.
ABSTRACT
Objective To observe the intervention effect of Schisandrin B (Sch B) on cisplatin induced acute kidney injury (AKI) in mice and its possible mechanism.Methods Twenty-five BALB/c mice were randomly divided into blank control group, model group, low and high dose of Sch B intervention groups and Sch B control group. Olive oil with Sch B was administered by gavage at the dose of 20 mg/kg or 100 mg/kg for low and high dose of Sch B intervention groups respectively; olive oil with Sch B 100 mg/kg was applied by gavage to the Sch B control group; the same volume of olive oil was perfused into the gastric cavity in the blank control group and model group; the above measures in various groups were consecutively used for 5 days. On the 3rd day of the experiment, AKI mice model was established by intraperitoneal injection of cisplatin (20 mg/kg) once and the same measure was given to the low and high dose of Sch B intervention groups; 1 mL/kg normal saline was injected into the peritoneal cavity in the bland control group and Sch B control group. At the end of the experiment, the serum creatinine (SCr) level was determined; apoptosis of renal tubular epithelial cells were detected by using terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) assay; the morphological changes of renal tubular epithelial cells were observed by hematoxylin eosin (HE) staining, and renal tubular injury score was evaluated; p53 protein content in the kidney tissue was measured by immunohistochemical analysis; furthermore, expressional level of p53 protein in renal tissue was tested by Western Blot.Results Compared with the blank control group, the level of SCr (μmol/L: 86.77±10.97 vs. 14.37±0.81), renal tubular injury score (9.67±1.20 vs. 1.00±0.45), the count of apoptotic renal tubular epithelial cells (cells/200 power field: 20.00±2.13 vs. 2.30±0.40) in the model group were all increased (P < 0.05 orP < 0.01), and p53 protein content (cells/400 power field: 13.40±2.66 vs. 57.30±3.82), and the expression of p53 protein [absorbency (A value) ratio: 0.79±0.09 vs. 1.42±0.09] in model group were decreased (bothP < 0.01). Compared with the model group, in the low and high dose Sch B intervented groups, the level of SCr (μmol/L: 21.98±5.52 and 37.45±5.04), renal tubular injury score (5.67±0.76 and 6.17±0.65), the count of apoptotic renal tubular epithelial cells (cells/200 power field: 10.60±1.05 and 11.60±1.45) were all reduced (allP < 0.01), p53 protein content (cells/400 power field: 42.40±3.67 and 45.90±2.31) and the expression of p53 protein (A value ratio: 1.36±0.16 and 1.25±0.11) were increased (bothP < 0.01). HE staining showed the pathological changes of renal tubules, such as renal tubular epithelial cellular fusion, vacuolization, cast formation, and tubular lumen constriction/dilation in model group; the pathological changes in kidney tissues observed in low and high dose Sch B intervention groups were milder than those in model group.Conclusion Sch B plays a beneficial role in the cisplatin induced AKI in mice, and its protective effect might be mediated by decreasing SCr, regulating p53 protein expression level and inhibiting the apoptosis of renal tubular epithelial cells.
ABSTRACT
@#Necroptosis is a newly discovered form of programmed cell death, which is activated by the binding of death receptors and their ligands and executed through specific path ways. At present, this form of cell death has been proved to be involved in a variety of diseases,such as cancer, autoimmune diseases, traumatic brain injury and brain ischemia-reperfusion injury.
ABSTRACT
@#ObjectiveTo observe the effect on repairing facial nerve injury of rabbits by neural stem cells and autologous fasia. Methods22 rabbits with transected facial nerve were divided into 2 groups randomly, control group (8 rabbits,15 sides totally), which transected facial nerve were wrapped by autologous fasia, and treament group (14 rabbits, 20 sides totally), which were wrapped by neural stem cells and autologous fasia. Six weeks after transplantation, neuro-electrophysiological test, immunohistochemical examination were done. The number and thickness of myelin in the re-connected area of transected facial nerve were observed. ResultsThe transplanted animals recovered much better than that in control group (P<0.05). Immunohistochemical examination showed a great deal of BrdU positive cells around the re-connected area of transected facial nerve. Immunohistochemical staining also found plenty of regenerative myelins in this area in the treatment group. While in control group, there were no BrdU positive cells and only a few of regenerative myelins in the same area. ConclusionTransplantation of neural stem cells combined with autologous fasia might become the new method to treat facial nerve injury.
ABSTRACT
Objective To investigate the causes and treatment of recurrent laryngeal nerve (RLN) injury during the operation of thyroidectomy. MethodsClinical data of 48 patients that RLN were injured during thyroidectomy in and out of our hospital from Jun. 2003 to Mar. 2007 were reviewed. ResultsNo patient died while operation and staying in hospital. There were 47 cases of unilateral RLN injury, 1 case of bilateral RLN injury; 21 cases (43.7%) were injured because of suture or scar adhesion, 13 cases (27.1%) were partly broken with formed scar, 14 cases (29.2%) were completely cut off; The locations of RLN injuries were closely adjacent to the crossing of the inferior thyroid artery and RLN in 13 cases (27.1%) and 35 cases (72.9%) were within 2 cm below the point of RLN entering into throat. The injured RLN were repaired surgically in 43 cases, among which 39 cases’ phonation and vocal cord movement were restored completely or had their vocal cord movement recovered partly; There were only 4 cases that the phonation and vocal cord movement were not recovered. Another 5 cases that did not take any repair did not recovered naturally. ConclusionThe location of most RLN injuries caused by mechanical injury during thyroid surgery is closely adjacent to the entrance of RLN into throat. Early nerve exploratory operation should be performed once the RLN is injured, and the method of repair should be decided according to concrete conditions of injury.
ABSTRACT
Objective To observe the effect of the injection of myoblast carrying human insulin-like growth factor-1(hIGF-1) on the expression of endogenous IGF-1 mRNA and IGF-1 level in mice skeletal muscle following injury.Methods Seventy two male C3H mice(20~30g,7~11w)were randomly divided into three groups(24 mice in each group) with four mice normal controls.Applied a falling hit from certain height at the medial calf of right lower limbs in three groups,the injured skeletal muscle model was successfully simulated.Three days following injury,the mice in group A and B were injected with 1?106 myoblasts either carried with or without hIGF-1 gene respectively and the mice in group C were injected with 100?l saline at the injured muscle.Three mice in each group were sacrificed randomly at day 2,5,10,15,20,30 after contusion.The expression level of mIGF-1 was assessed by immunohistochemical staining and real time PCR.Results mIGF-1 mRNA expression and mIGF-1 factor secretion were observed in all three groups;the amount of mIGF-1 mRNA expression and mIGF-1 secretion in group A were significant higher than that in group B and C.Conclusion Myoblast carrying hIGF-1 transplantation could promote endogenous IGF-1 secretion in injured skeletal muscle.
ABSTRACT
The finger flexor injuries are very difficult to treat satisfactorily. It is usually said that the earlier the treatment performed, the better result obtained. But the delicasy of the hand anatomy and its function as well as the absence of the hand surgeon in the first aid care make the problem more complex. Even if we made the primary treatment to the flexor tendon injuries, some disabilities are often remained. We have treated fifty eight cases of old flexor tendon injuries in forty eight patients, the results can be summarized as follows. 1. The cause of the tendon damage is due to the laceration injury in the majorities of the cases. T,he tendon injuries are especially common between the late second and the early third decade. 2. In the injury of the Zone II with pulley distortion, the pulley reconstruction using palmaris longus or fascia from other sites will prevent bowstring and help the tendon function. 3. The Zone II can be subdivided into two subspecific areas. The proximal area is from the distal palmar crease to the midoprtion of porximal phalanx and the distal one is from the midportion of the proximal phalanx to the insertion of the sublimis tendon. In the proximal area one can repair the injured tendon directly after removal of the A1 and about proximal half of the A2 pulley without any subsequent bowstring if the tendon and its tunnel is relatively well preserved. Thus one can convert this proximal portion of Zone II to Zone III. So the proximal area of the Zone II should be differentiated from the remaining distal part of the Zone II. 4. At six months after the operation the result of the operation was analyzed by the percentage of the recovery, which was calculated by the postoperative active range of the interphalangeal joints divided by one hundred seventy five degrees that means the available total range of motion of normal interphalangeal joints. Excluding the cases with the tenodesis or arthrodesis, the total result revealed good or excellent in about ninty percentages with this method. 5. There were two fingers that showed a postoperative lumbrical plus state in Zone II, which were recovered spontaneously within three to four months postoperatively. So it is considered that the relative shortening of the lumbrical muscles can be treated and overcome conservatively by the active use of the fingers, and there is no need to perform an lumbrical tenotomy to correct this kind of muscle imbalance.
Subject(s)
Humans , Arthrodesis , Fascia , Fingers , First Aid , Hand , Joints , Lacerations , Methods , Muscles , Patella , Patellar Ligament , Range of Motion, Articular , Tendon Injuries , Tendons , Tenodesis , Tenotomy , TibiaABSTRACT
Objective To observe the survival of myoblasts carrying hIGF-1 gene transplanted into the mice, and the expression of hIGF-1 in the transplanted mice. Methods Eighty four male C3H mice(20～30g,7～11w)were divided into four groups: group A, B, C and D (20 mice each group), and the remaining four mice were used as normal control. At the middle of the right gastrocnemius muscle, the mice in group A and B were injected with 1?10~6 myoblasts either carried with or without hIGF-1 gene. Muscle contusion at the middle of the right gastrocnemius muscle of the mice in group C and D was produced. At day 3 following injury, they were injected with 1?10~6 myoblasts either carried with hIGF-1 gene (group C) or without hIGF-1 gene (group D). At the day 2, 5, 10, 20, 30 after injection, four mice of each group were sacrificed randomly. BrdU staining in all mice were performed to evaluate cells surviving, and the expression level of hIGF-1 in group A and C was assessed by immunohistochemical staining and real-time-PCR. Results The BrdU staining in both normal and injured mice transplanted with myoblast carried with or without hIGF-1 were positive. hIGF-1 was expressed and secreted in both group A and C. Conclusion The myoblast carrying hIGF-1 gene transplanted into normal or injured mice can survive for a certain period of time, and can secrete hIGF-1.