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AIM:To investigate the effects of astragalin(AST)on activation status of astrocytes and the ex-pression level of autophagy-related proteins in the cortex of the anterior cingulate cortex of mice with a complete Freund's adjuvant(CFA)-induced inflammatory pain model.METHODS:Twenty-four 6-month-old male C57BL/6 mice were ran-domly divided into four groups:control group,saline group,CFA model group and CFA+60 mg/kg AST administration group,and six mice in each group.Mice in the AST administration group received 60 mg/kg AST by intraperitoneal injec-tion on a body weight basis for 21 d.The paw withdrawal threshold in each group of mice was evaluated by the von Frey test.The expression levels of autophagy-related factors LC3,p62,ATG12 and beclin-1,and astrocyte activation were de-tected by multiplex immunofluorescence staining in the anterior cingulate cortex of mice in each group.Western blot was used to measure the levels of autophagy-related proteins LC3,p62,ATG12 and beclin-1 in the anterior cingulate cortex of mice in each group.RESULTS:Behavioural tests showed that AST significantly increased mechanical pain thresholds in CFA mice(P＜0.05).The results from multiple immunofluorescent staining showed that AST significantly increased the fluorescence intensity of LC3(P＜0.01),ATG12(P＜0.01)and beclin-1(P＜0.05),attenuated the fluorescence intensi-ty of p62(P＜0.05),and inhibited the activation of astrocytes in the anterior cingulate cortex of CFA mice.Western blot results further confirmed that AST significantly increased the expressions of LC3(P＜0.01),ATG12(P＜0.01),beclin-1(P＜0.01),and decreased the expression of p62(P＜0.05)in the anterior cingulate cortex of CFA mice.CONCLU-SION:AST relieves CFA-induced inflammatory pain of mice,and its analgesic mechanism may be related to the inhibi-tion of activation of cortical astrocytes in the anterior cingulate cortex and the promotion of autophagy in CFA mice.
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Objective To investigate the neurodevelopmental toxicity of ACR by studying the expression of DCX and GAP-43 in the hippocampal dentate gyrus of rats after maternal exposure to acrylamide. Methods Pregnant rats were randomly divided into low-dose ACR(4.5 mg/kg),medium-dose(9 mg/kg),high dose groups(18 mg/kg)and the control group(0 mg/kg),8 in each group,and were exposed to toxicant from gestation-al day 15 to postnatal day 13. All rats and their pups were killed on postnatal day 14. ABC immunohistochemistry was used to detect the expression of GFAP in the hippocampus of mother rats and offspring. Results Compared with the control group,the expression of DCX and GAP-43 in hippocampus dentate gyrus of the pregnant rats in middle and high dose groups was significantly decreased(P < 0.05). Conclusion ACR may interfere with the growth and development of neurons by reducing the expression of DCX and GAP-43.
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[Objective] The present study aimed to determine the protective role of Melatonin (MT) against Acrylamide (AA)-induced testicular toxicity and the potential molecular mechanism.[Methods] The animals were randomly divided into three groups,the control group (n =12),the AA group (n =12) and the AA+MT group (n =12).The rats in the AA and AA + MT group were gavaged with AA at a dose of 15 mg/(kg · day) for 4 consecutive weeks.After 3 weeks of AA treatment,MT was intraperitoneally injected 30 minutes before AA treatment at 10 mg/(kg· day) for 1 week in the AA + MT rats.Subsequently,the mitochondrial membrane potential measurement,TUNEL assay,Western blot and electron microscopic techniques were applied in the present study.[Results] The results showed that AA could decrease the testis mitochondrial membrane potential (P ＜ 0.05) which could be recovered by MT (P ＜ 0.05).Moreover,MT induced down-regulation of Bax expression and up-regulation of Bcl-2 expression in the testis,compared with AA rats.The amelioration of testicular apoptosis was further confirmed by the TUNEL labeling.Western blot results suggested that the decreased ratios of Bcl-2/Bax and Bcl-xL/Bak in the AA group (both P ＜ 0.05) could be recovered by MT treatment (both P ＜ 0.05).The levels of Cyt-c,Casp-3,p53 and NF-κB in AA group were markedly elevated compared with the control (all P ＜ 0.05),and reduced in MT treatment group (all P ＜ 0.05).MT could relieve abnormal mitochondrial structures in the seminiferous tubule in the electron microscopic level.[Conclusion] MT may exert productive effect through its anti-apoptotic properties associated with mitochondria.
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<p><b>OBJECTIVE</b>To investigate the seasonal variation of total flavonoid content of Farfugium japonicum and its response to stress.</p><p><b>METHODS</b>The total flavonoids of Farfugium japonicum were determined by spectrophotometry in different seasons and under various stressful factors.</p><p><b>RESULTS</b>The total flavonoid content in Farfugium japonicum leaves was the highest, followed by the petiole, and rhizomes (P<0.05). The total flavonoid content in the leaves in December was higher than that in other months; that in the petiole and rhizome fluctuated in different seasons (P<0.05). As the light intensity enhanced, the total flavonoids in Farfugium japonicum leaves, petioles, rhizomes showed a downward trend. With the increase of water stress, the total flavonoid content in Farfugium japonicum leaves gradually increased, that in petiole first increased and then decreased,while that in rhizomes decreased (P<0.05). With the salt stress, the total flavonoid content in leaves, petioles and rhizomes of Farfugium japonicum showed a decreasing trend (P<0.05). With the increasing of temperature, the total flavonoid content in the leaves showed a gradually increasing trend; that in petiole first decreased and then increased,while that in the rhizomes first increased and then decreased (P<0.05).</p><p><b>CONCLUSION</b>The total flavonoids of Farfugium japonicum fluctuate with the change of seasons and that in different parts of the plant has different responses to ecological stressful factors.</p>
Sujet(s)
Asteraceae , Chimie , Flavonoïdes , Saisons , Stress physiologiqueRÉSUMÉ
Objective To investigate the expression of neuron-specific enolase(NSE) and bone morphogenic protein 4(BMP4) in different hippocampal areas of pentylenetetrazol(PTZ) kindled epilepsy rats and explore their relationship with the pathogenesis of epilepsy and brain injury.Methods Fifty male SD rats were divided into experimental group(n=40) and control group(n=10).The rats in experimental group were kindled into epilepsy by chemical method,and according to the kindling process,subdivided into four groups(grade Ⅰ,Ⅲ,Ⅳ,Ⅴ).Immunohistochemistry,in situ hybridization labeled with Dig-oligonucleotide probe and the image analyzing system were used to observe the expressions of NSE and BMP4 in rat hippocampus.Results In PTZ kindled epilepsy rats,the number of cells positive for NSE and BMP4 was increased in many regions of hippocampal formation.Compared with control group,the expressions of NSE and BMP4 in CA3 and DG was elevated obviously in the grade Ⅲ group and grade Ⅳ group(P