Objective To assess the effectiveness and safety of Weifuchun for chronic atrophic gastritis. Methods Trials were located through electronic searches of The Cochrane Library (Issue 3, 2007), EMbase (1974 to June 2007), PubMed (1966 to June 2007), CBM (1978 to June 2007), CNKI (1994 to June 2007) and VIP (1989 to June 2007). Randomized controlled trials (RCTs) and quasi-RCTs of Weifuchun for chronic atrophic gastritis were included. A critical quality assessment and Meta-analysis were performed for the included studies. RevMan 4.2.2 was used for statistical analysis. Results A total of 8 trials involving 816 patients were included. Meta-analysis showed that compared with the control group, Weifuchun for the CAG treatment group had superiority in many aspects such as effective rate according to Gastroscopy (RR 1.54 and 95%CI 1.31 to 1.81), effective rate according to Patho-check (RR 1.99 and 95%CI 1.54 to 2.58), adverse events, remission rate based on clinical symptoms (RR 1.47 and 95%CI 1.30 to 156), remission rate based on a single symptom, curative effect with IM/ATP, HP darkening rate (RR 1.26 and 95%CI 1.02 to 1.56), situation of hemoglobin change and so on. No RCTs were found to describe the safety of Weifuchun for CAG. Conclusion Because of low quality and small samples, there is no enough evidence on Weifuchun for chronic atrophic gastritis. More largescale multi-center randomized trials are needed to investigate the role of Weifuchun for chronic atrophic gastritis.
Objective To provide the anatomical basis of contralateral C7 root transfer for the recovery of the forearm flexor function. Methods Thirty sides of adult anti-corrosion specimens were used to measure the length from the end of nerves dominating forearm flexor to the anastomotic stoma of contralateral C7 nerve when contralateral C7 nerve transfer was used for repair of brachial plexus lower trunk and medial cord injuries. The muscle and nerve branches were observed. The length of C7 nerve, C7 anterior division, and C7 posterior division was measured. Results The length of C7 nerve, anterior division, and posterior division was (58.8 ± 4.2), (15.4 ± 6.7), and (8.8 ± 4.4) mm, respectively. The lengths from the anastomotic stoma to the points entering muscle were as follow: (369.4 ± 47.3) mm to palmaris longus, (390.5 ± 38.8) mm (median nerve dominate) and (413.6 ± 47.4) mm (anterior interosseous nerve dominate) to the flexor digitorum superficialis, (346.2 ± 22.3) mm (median nerve dominate) and (408.2 ± 23.9) mm (anterior interosseous nerve dominate) to the flexor digitorum profundus of the index and the middle fingers, (344.2 ± 27.2) mm to the flexor digitorum profundus of the little and the ring fingers, (392.5 ± 29.2) mm (median nerve dominate) and (420.5 ± 37.1) mm (anterior interosseous nerve dominate) to the flexor pollicis longus, and (548.7 ± 30.0) mm to the starting point of the deep branch of ulnar nerve. The branches of the anterior interosseous nerve reached to the flexor hallucis longus, the deep flexor of the index and the middle fingers and the pronator quadratus muscle, but its branches reached to the flexor digitorum superficials in 5 specimens (16.7%). The branches of the median nerve reached to the palmaris longus and the flexor digitorum superficial, but its branches reached to the deep flexor of the index and the middle fingers in 10 specimens (33.3%) and to flexor hallucis longus in 6 specimens (20.0%). Conclusion If sural nerve graft is used, the function of the forearm muscles will can not be restored; shortening of humerus and one nerve anastomosis are good for forearm flexor to recover function in clinical.
Objective To investigate the effect of Ligustrazine on the expressions of FoXO3a, MAFbx, and MuRF1 indenervated skeletal muscle atrophy rats. Methods Fifty-four 8-week-old female Sprague Dawley rats were randomly dividedinto 3 groups: normal control group (group A, n=6), denervated control group (group B, n=24), and Ligustrazine interventiongroup (group C, n=24). After the denervated gastrocnemius models were established in the rats of groups B and C, sal ine andLigustrazine [80 mg/(kg·d)] were given every day by intraperitoneal injection, respectively. However, no treatment was donein group A. At 2, 7, 14, and 28 days after denervation, the wet weight of gastrocnemius was measured to calculate the ratio ofwet weight. The mRNA and protein expression levels of FoXO3a, MAFbx, and MuRF1 were detected by RT-PCR and Westernblot. Results The ratio of gastrocnemius wet weight decreased with time after denervation in groups B and C, showingsignificant differences when compared with that of group A (P lt; 0.05), and group C were significantly higher than that of groupB at 7, 14, and 28 days (P lt; 0.05). The mRNA and protein expressions of FoXO3a, MAFbx, and MuRF1 in groups B and Cwere significantly higher than those in group C at 7, 14, and 28 days (P lt; 0.05), and group C was significantly lower than groupB (P lt; 0.05). Conclusion Ligustrazine may postpone denervated skeletal muscle atrophy by reducing mRNA and proteinexpressions of FoXO3a, MAFbx, and MuRF1.
Objective To investigate the preventive and therapeutic effects and the mechanisms of pyrrol idine dithiocarbamate (PDTC) on the atrophy of denervated skeletal muscle. Methods Thirty adult Wistar rats of either gender, weighing (200 ± 10) g were randomly divided into 3 groups: group A (n=6, control group), group B (n=12, denervation group), and group C (n=12, PDTC treatment group). The sciatic nerves of the rats were only exposed without cutting off in group A, and the rats were made denervated gastrocnemius models in groups B and C. PDTC of 100 mg/(kg•d) was injected peritoneally in group C and an intraperitoneal injection of the same amount normal sal ine was given in group B. After 14 and 28 days, the gastrocnemius was harvested to measure the ratio of muscle wet weight; the levels of nuclear factor of κB (NF-κB)p65 protein and the opening of the mitochondrial permeabil ity transition pore (MPTP) in the gastrocnemius were detectedrespectively by Western blot and laser confocal scanning microscope; and the apoptotic cells in atrophic muscle were measured with TUNEL. Results The ratio of muscle wet weight in group A was 1.039 ± 0.115, and it significantly decreased in groups B and C (P lt; 0.05); after 14 and 28 days of operation, the ratio of muscle wet weight in group C significantly increased when compared with those in group B (P lt; 0.05). The expression of NF-κB p65 protein in group A was 0.224 ± 0.041; the expressions of NF-κB p65 in groups B and C significantly increased when compared with that in group A (P lt; 0.05); however, the expression of NF-κB p65 in group C was significantly lower than that in group B (P lt; 0.05). The MPTP fluorescence intensity in group A was 31.582 ± 1.754; the MPTP fluorescence intensity was significantly lower in groups B and C than in group A (P lt; 0.05), and the MPTP fluorescence intensity in group C was significantly higher than that in group B (P lt; 0.05). The rate of apoptosis in group A was 4.542% ± 0.722%; after 14 and 28 days of operation, the rates of apoptosis significantly increased when compared groups B and C with group A, and signiticantly decreased when compared group C with group B (P lt; 0.05). Conclusion PDTC can retard denervated skeletal muscle atrophy, and the effect may have a relationship with its inhibition on NF-κB, the opening of the MPTP, and the ratio of apoptosis.
Objective To investigate the expression of micro-dystrophin gene in myoblast cultured in vitro, to explore the possibil ity of combining myoblast transplantation with gene transfer for Duchenne muscular dystrophy therapy. Methods Competent Escherichia coli JM109 was prepared, which transformed with plasmid pSL139, and positive clones were picked to cultivate. Plasmid was extracted with Alkal ine lysis method and cutted with both Pvu I and Cla I enzyme. Agarose gel electrophoresis was employed to take pictures. Ten healthy 5-7 days old male C57/BL10 mice were selected, weighing4-5 g, the primary and subcultured myoblasts were cultured with multi-step enzymatic digestion and differential adhesionmethod, and Desmin immunofluorescent method was used to identfy. The 3rd generation myoblasts that were transfected with plasmid pSL139 mediated by l iposome served as the experimental group, untransfected cells served as the control group. After 48 hours of transfection, the expressions of micro-dystrophin mRNA and protein in myoblasts were detected with RTPCR and cell immunofluorescent methods, and the transfection efficiency was caculated. Results After pSL139 plasmids being digested and for 40 minutes agarose gel of electrophoresis, 3.75 kb fragment of target gene and vector were observed. The cells were almost uniform, and triangular or diamond shape after 24-48 hours of culture; the cells turned to fusion manner and could be passaged after 4-6 days. Desmin immunofluorescent result showed that green fluorescence was seen in cytoplasm of most 2nd myoblasts, and the purity of the myoblasts was above 90%. At 48 hours after transfection of myoblasts with plasmid pSL139, RT- PCR results showed that about 300 bp fragment was seen in the experimental group and the control group, and the brightness was higher in experimental group. Immunofluorescent staining displayed that green fluorescence was seen in the cytoplasm of the myoblasts in the experimental group and no green fluorescence in the control group; the expression efficiency of positive cells for micro-dystrophin was 45%-55% in experimental group. Conclusion Micro-dystrophin gene can highly express at the levels of mRNA and protein respectively in myoblasts transfected with plasmid pSL139 mediated by l iposome.
Objective To analyze the expression changes of Pax7 and MyoD in satell ite cells of denervated skeletal muscle at the mRNA and protein level, and to explore the pathway concerning with denervation and regeneration of skeletal muscle. Methods Nine male SD rats of 2 months old, weighing 180-200 g were selected. The right gastrocnemius musclewas made denervation model as experimental sides, and the same operation was performed in the left sides as control. The immunofluorescence analysis was done for detecting the protein expressions of Pax7 and MyoD in muscles denervated 3, 7 and 21 days after operation. The RT-PCR analysis was used to explore the mRNA expression of MyoD and Pax7 in extracted tissues from denervated muscles. Results Nine rats survived after operation, with l imited motion of right hind l imbs, and normal motion of left l imbs. The result of immunofluorescence with the polyclonal antibody against MyoD and the monoclonal antibody against Pax7 showed that the number of MyoD positive cells in prolonged denervated muscles (experimental sides) increased gradually, and reached the peak 21 days after denervation, there was significant difference compared with that of control sides (P lt; 0.05). However, the total number of Pax7 positive cells decreased with the prolongation of denervation, the expression of Pax7 was b only at 3 days, then decreased gradually, and there was no positive cells in denervated muscles of 21 days. There were significant differences in Pax7 positive cells between experimental sides and control sides at 3 and 7 days (P lt; 0.05). The results of immunostaining showed that MyoD mRNA levels increased , and reached the peak at 21 days of denervation, there was significant difference compared with that of control sides (P lt; 0.05). Whereas, Pax7 mRNA expressed only in control, denervated muscles of 3 and 7 days, and its expression level decreased gradually. Conclusion One possible reason of the depletion of satell ite cell pool in prolonged denervated muscle is the down-regulation of Pax7.
Objective To explore the effect of tri pterygium glycoside (TG) on the skeletal muscle atrophy and apoptosis after nerve allograft. Methods Twenty Wistar male rats were adopted as donors, weighing 200-250 g, and the sciatic nerves were harvested. Fifty SD male rats were adopted as recipients, weighing 200-250 g. Fifty SD rats were made the models of10 mm right sciatic nerve defect randomly divided into five groups (n=10): group A, group B, group C, group D and group E.groups A and B received fresh nerve allograft, groups C and D received sciatic nerve allograft pretreated with TG, and group E received autograft. The SD rats were given medicine for 5 weeks from the second day after the transplantation: groups A and E were given physiological sal ine, groups B and D TG 5 mg/ (kg·d), and group C TG 2.5 mg/ (kg·d). At 3 and 6 weeks, respectively, after nerve transplantation, general observation was performed; the structure of skeletal muscles was observed by HE staining; the diameter of skeletal muscles was analyzed with Image-Pro Plus v5.2; the ultrastructure of skeletal muscles was observed by TEM; the expressions of Bax and Bcl-2 were detected by immunohistochemical staining; and the apoptosis of skeletal muscles was detected by TUNEL. Results All rats survived to the end of the experiment. In general observation, the skeletal muscles of SD rates atrophied to different degrees 3 weeks after operation. The muscular atrophy in group A was more serious at 6 weeks, and that in the other groups improved. The wet weight, fiber diameter and expression of Bcl-2 in group A were significantly lower than those in groups B, C, D and E (P lt; 0.01)；those in groups B, C and D were lower than those in group E (P lt; 0.05); and there were no significant differences among groups B, C and D (P gt; 0.05). The apoptosis index and expression of Bax in group A were significantly higher than those in groups B, C, D and E (P lt; 0.01)；those in groups B, C and D were higher than in groupE (Plt; 0.05); and there were no significant differences among groups B, C and D (P gt; 0.05). Three weeks after nerve allograft, under the l ight microscope, the muscle fibers became thin; under the TEM, the sarcoplasmic reticulum was expanded. Six weeks after nerve allograft, under the l ight microscope, the gap of the muscle fibers in group A was found to broaden and connective tissue hyperplasia occurred obviously; under the TEM, sarcomere damage, serious silk dissolution and fragmentary Z l ines were seen in group A, but the myofibrils were arranged tidily in the other groups, and the l ight band, dark band and sarcomere were clear. Conclusion TG can decrease the skeletal muscle atrophy and apoptosis after nerve allograft. The donor’s nerve that is pretreated with TG can reduce the dosage of immunosuppressant for the recipient after allograft.
Objective To investigate the effect of exogenous erythropoietin (EPO) on the denervated muscle atrophy. Methods Twenty-four SD male rats, weighting 200-220 g were made the models of denervated gastrocnemius muscle after sciatic nerves were transected under the piriform muscle at the right lower leg, and were randomly divided into two groups (n=12). rhEPO (2 500 U/kg) was injected daily into the denervated gastrocnemius muscle in EPO group, and normal sal ine was injected into the denervated gastrocnemius muscle in control group. To observe the general state of health of the experimental animal, the muscle wet weight, the muscle cell diameter, the cross section area, the protein amount, thepercentage of the apoptotic muscle cells, and the Na+-K+-ATPase and Ca2+-ATPase activities were measured 2 and 4 weeks after operation. Results All experimental animals were survived during experiment without cut infection, and all animals could walk with pull ing the right knee. At 4 weeks after operation, 7 cases showed ulcer in the right heel, inculding 5 in the control group and 2 in the EPO group. At 2 and 4 weeks after operation, the muscle wet weight in EPO group was (885.59 ± 112.35) and (697.62 ± 94.74) g, respectively; in control group, it was (760.63 ± 109.05) and (458.71 ± 58.76) g, respectively; indicating significant differences between two groups (P lt; 0.01). The protein amount in EPO group was (77.37 ± 5.24) and (66.37 ± 4.87) mg/mL, respectivly；in control group, it was (65.39 ± 4.97) and (54.62 ± 6.32) mg/mL；indicating significant differences between two groups (P lt; 0.01). At 2 and 4 weeks after operation, the myofibrillar shapes were nearly normal in EPO group while there were muscle fiber atrophy, some collapse and obviously hyperblastosis between muscle bundle. There were significant differences in the muscle cell diameter and the cross section between two groups (P lt; 0.01). However, the percentage of the apoptotic muscle cells was 11.80% ± 1.74% and 28.47% ± 1.81% in control group, respectively, which was significantly smaller than that in EPO group (21.48% ± 2.21% and 55.89% ± 2.88%, P lt; 0.01). At 2 and 4 weeks after operation, Na+-K+-ATPaseand Ca2+-ATPase activities in EPO group were higher than those in control group (P lt; 0.01). Conclusion EPO can delay the denervated muscle atrophy.