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BackgroundSkeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.MethodsWe generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.ResultsMAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.ConclusionMondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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BackgroundSkeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.MethodsWe generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.ResultsMAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.ConclusionMondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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Objective@#To investigate the effect of intestinal flora in children with functional constipation (FC) on expression of acid-sensitive Ion channel 3(ASIC3) in rats and their regulation in intestinal motility.@*Methods@#Faeces of FC children identified according to RomeⅣ criteria and healthy children from the First Affiliated Hospital of Anhui Medical University from December 2017 to June 2018 were collected, and then made into fecal microbiota solution.A pseudo - sterile rat model was established, according to the random number table method, and the rats were randomly divided into the treatment group and the control group, with 12 rats in each group, then the treatment group was given fecal microbiota solution of the children with FC and the control group was given fecal microbiota solution of the healthy children.The visceral sensitivity and intestinal propulsion rate of rats were determined by means of abdominal withdrawal reflex (AWR), while the intestinal microorganism of rats and children with FC were determined by 16SrDNA high-throughput sequencing, and the expressions of ASIC3 of intestinal in mRNA and protein were determined by adopting fluorescence quantitative PCR and Western blot.@*Results@#The species and quantity of intestinal flora of the children with FC and rats implanted with FC faecal bacteria were reduced(all P<0.05), and firmicutes and bacteroidetes were the main bacteria; compared to the control group, the small intestine propulsion rate(52% vs.74%) and visceral sensitivity(78 mmHg vs.63 mmHg) of the treated group were significantly decreased compared with those in the control group (all P<0.05); the mRNA (0.003 1±0.000 8 vs.0.012 4±0.002 5) and protein levels of ASIC3 (0.013 2±0.001 9 vs.0.072 1±0.008 7) in the small intestine were down-regulated significantly(all P<0.05); and the mRNA (0.002 8±0.000 7 vs.0.009 4±0.001 1) and protein levels of ASIC3(0.038 2±0.004 5 vs.0.089 7±0.009 4) in the colon were down-regulated significantly(all P<0.05).@*Conclusions@#Children with FC have intestinal flora disorder, and intestinal flora of FC children may affect intestinal motility by down-regulating the expression of intestinal ASIC3 in rats.
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<p><b>OBJECTIVE</b>To explore the material basis of conduction along meridian.</p><p><b>METHODS</b>Sixty SD rats(30 males,30 females) were randomly assigned into a normal group,an acupuncture group,a verapamil blocking group and a 0.9%NaCl blocking group(control group),15 rats in each one. Fluo 3-AM(calcium fluorescence probe) was injected at the observation part in femoral stomach meridian of foot-(meridian part) and the approaching femoral meridian part(non-meridian part) in the normal group and the acupuncture group,and then incubation was applied. In the verapamil blocking group,verapamil was injected at local meridian part and non-meridian part,and in the control group 0.9%NaCl was injected. Then Fluo 3-AM was injected at the meridian part and non-meridian part in the two groups,and incubation was implemented. Caimaging changes in cells were recorded for more than 20 min after injection of every part in each group respectively. After the above operations in the last three groups,acupuncture was used at "Zusanli"(ST 36) immediately,with electroacupuncture for one min,then Caimaging changes in cells at the meridian and non-meridian parts were recorded for more than 20 min.</p><p><b>RESULTS</b>In the normal group, Cafluorescence intensity at the meridian part was higher than that at the non-meridian part. In the acupuncture group,after acupuncture Cafluorescence intensity at the meridian part was obviously higher than before,but the change before and after acupuncture was not apparent at the non-meridian part. After verapamil blocking local calcium channel and acupuncture,the Cafluorescence of the meridian part did not strengthen,and the change of that before and after acupuncture at the non-meridian part was not obvious. In the control group,after injecting 0.9%NaCl at local part,Cafluorescence intensities of the meridian and non-meridian parts showed no obvious change,so was that before and after acupuncture.</p><p><b>CONCLUSIONS</b>The voltage-gated calcium channel at the meridian part is highly correlated with its tissue cells exciting conduction.</p>
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Objective:To investigate the effects of chronic anger stress on rats' aging process and the mechanism of the neuroendocrine-immune network. Methods:After the aging and brain aging rats induced by D-galactose(D-gal) were stimulated by anger, observation of the effects of chronic anger stress on the rats' spatial learning and memory was made, the contents of norepinephrine(NE), 5-hydroxytryptamine(5-HT)in brain tissue and serum, the levels of adrenocorticotropic hormone (CORT) in serum were assayed, the spleen index was measured. Results:Compared with the D-gal group, in the D-gal group stimulated by anger, the rats' ability of spatial learning and memory declined, the contents of NE in brain tissue and serum increased, the contents of 5-HT declined, the levels of CORT in serum increased, and the spleen index declined. Conclusion: The rats' aging and brain aging were aggravated and the aging process were accelerated by chronic anger stress. The possible mechanism were the sustained excitability of the HPA axis and SAS, disturbances of neuroendocrine system and immunological function repression.
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AIM: To study the mechanism of myocardial injury after brain ischemia-reperfusion in aged rats from the changes in Dopamine (DA), Noradrenalin (NE), Epinephrine(E) and Neuropeptide Y(NPY).METHODS: Young (5 months) and aged (20 months or more) rats were divided into model groups and normal control groups, respectively. We observed the following items in rats with 60 minute reperfusion after 30 minute brain ischemia: the pathological changed of myocardium, the activities of lactic dehydrrogenase(LDH), creatine phosphokinase(CPK), the contents of NE, DA, E, NPY. RESULTS:The CPK and LDH activities in the young model rats were higher than those in the young control rats was higher than that in the young control rats (P＜0.05). The serum CPK activity in the aged control rats was higher than that in the young control rats (P＜0.05). The myocardial CPK activity was higher in the aged model rats compared with the young molel rats (P＜0.05) and was higher in aged control rats compared with the young control rats (P＜0.01). The myocardial LDH activity was lower in the aged control rats than that in the young control rats (P＜0.05) and aged model rats (P＜0.01). The serum NE level, the level of NE and DA in the hypothalamus were higher obviously than those in the young control rats. The serum NE contents in the two model groups (young and aged) were higher respectively than the two control rats (young and aged). The following items’ contents were higher in the aged model rats than in the young model rats: serum NE, serum E, hypothalamus NE. The hypothalamus NE and E content was lower in the aged model rats than in te aged control rats. NPY level in the brain tissue was lower in the aged control rats than that in the young control rats and aged model rats (P＜0.05).CONCLUSION: The myocardial injury after brain ischemia-reperfusion was concerned with the enhanced excitability of sympathetic-adrenal system, espectially in the aged rats. However, the change in myocardial enzyme was not serious in the aged rats compared with young rats.
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AIM: To study the protecitve mechanism of Ligustrazine (LT), Shenmai Parenteral Injection (SPI), combination of Ligustrazine and Shenmai Parenteral Injection (LSP) to myocardial injury after brain ischemia-reperfusion in aged rats from the change in ATPase and free radical in order to provide theoretical basic for prevention and cure of cerebral infarction. METHODS: Aged rats (more than 20 months) were divided into model group, control group, Nimotop group, LT group, SPI group and LSP group. We measured the following items in aged rats with 60 min of reperfusion after 30 min of brain ischemia: the content of MDA, the activities of superoxide dismutase (SOD), lactic dehydrrogenase (LDH), creatine phosphokinase (CPK), ATPase. RESUTLS: The CPK and LDH activities in the model rats increased obviously. The serum CPK activity in the LSP group, the LT group, nimotop group was lower than those in the model group obviously. The serum LDH activities in LT group and SPI group were obviously lower compared with those in the model group. The activity of Na＋-K＋-ATPase and Ca2＋-ATPase in model group was decreased. Contrast to the model group, the activity of Na＋-K＋-ATPase in LSP group, Nimotop group, LT group and the activities of Ca2＋-ATPase in the LSP group were higher. The serum MDA/SOD ratio was larger than that in the control group. The decrease in myocardial SOD activity and the increase in the MDA level, MDA/SOD ratio in the model group showed significant difference compared with that in the control. The MDA level in the LSP group was lower than that in the model group. The increase in myocardial SOD activity and decrease in MDA, MDA/SOD ratio were obvious in the LSP group compared with the model group. CONCLUSION: The myocardial injury after brain ischemia-reperfusion in aged rats was related to the decrease in the activity of Na＋-K+-ATPase and injury of free radical. LT, SPI, LSP and Nimotop could prevent this inury. Nimotop and LT could enhanced the activity of Na+-K+-ATPase obviously. SPI could enhance the activity of Ca2＋-ATPase and restrain the injury of free redical and lipid peroxidation. This may be the mechanism of restraining myocardial injury after brain ischemia-reperfusion.
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AIM: To study the mechanism of brain ischemia-reperfusion injury from ATPase activity and free radical metabolism in aged rats. METHODS: The young rats (5 months) and the aged rats (more than 20 months) were divided into young control group(YCG), young model group(YMG), aged control group(ACG) and aged model group(AMG). The ATPase and SOD activities and the contents of MDA, Ca 2+ , Na + and K + were measured in the rats with 30 min brain ischemia followed by 60 min reperfusion. RESULTS: The Ca 2+ content in the AMG was higher than that in the YMG and the ACG. The Na +-K +-ATPase activity in the ACG was lower than that in the YCG,was lower in the AMG than that in the YMG . The Ca 2+ -ATPase activities in the YCG was higher than that in the ACG, was lower in the AMG than that in the YMG and was higher than the ACG's. The serum and brain tissue SOD activities in the ACG was lower than that in the YCG, was lower in the AMG than YMG 's. The serum and brain tissue MDA/SOD ratio in the AMG was higher than that in the ACG. CONCLUSION: The brain tissue ischemia- reperfusion injury was related with calcium overload and free radical injury. The pathological changes were obvious and had some characteristics in the aged rats compared with the young rats because of the brain tissue aging changes in ATPase,calcium content and free radical metabolism in the aged rats.
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AIM\ To study the protective mechanism of ligustrazine(LT), shenmai injection(SI), combination of ligustrazine and shenmai injection (LSI) to injury of kidney after brain ischemia reperfusion in aged rats from the free radical change. METHODS Aged rats (more than 20 months) were divided into model group (Aged model), control group(Aged control), nimotop group(NG), ligustrazine group(LG), shenmai injection group(SIG) and LSI group(LSG). The following items was measured in aged rats with 60 min reperfusion after 30 min brain ischemia: the content of creatinine(Cr), urea nitrogen(BUN), MDA and the activitiy of superoxide dismutase(SOD). RESULTS The distinct pathological and functional injury in the kidney was found in the models, and this change was alleviated in each treatment group. The increase of MDA content in the models kidney tissue was obvious than that in the controls. The MDA level in the LG and the SIG was decreased. CONCLUSION The kidney injury after brain ischemia reperfusion in aged rats is correlated with the injury of free radical. LT, SI ,LSI and nimotop alleviate this injury. LT and SI restraine the injury of lipid peroxidation, this may be one of the mechanisms of restraining kidney injury after brain ischemia reperfusion.