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Objective To assess the quality of donor liver allografts by employing laser scanning confocal microscope (LSCM ) and clinical liver function tests .Methods Sprague-Dawley rats were used for establishing cold ischemia models of liver allografts .According to different timepoints of cold ischemia ,four groups of CIT1h ,CIT6h ,CIT12h and CIT24h were designated .At the end of cold ischemia time (CIT) of each group , perfusion and preservation fluids were collected and fluoresceins perfused . After LSCM examinations ,tissue samples were harvested for HE examination .Finally a comparison was made between LSCM results and hematoxylin & eosin (HE) examinations .Also some relevant clinical parameters were detected in preserving and flushing fluids .Results Both LSCM examination and pathological examination indicated that the quality of liver allografts decreased significantly with the elapsing of time . Only the difference of LDH was statistically significant (P<0 .001) .Conclusions LSCM may be used for evaluating the ex vivo qualities of liver allografts .Simple handling and time efficiency re great advantages of LSCM .As compared with alanine transaminase (ALT ) and aspartate transaminase (AST ) ,LDH is a better indicator reflecting the quality of liver allografts .
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Laser scanning confocal microscope (LSCM) has been used in the field of morphological research of acupuncture and moxibustion for more than 20 years. It is one of the important tools for revealing the structure of acupoints and the effect of acupuncture from histological perspective. With the help of technical advantages of LSCM, the quality of morphological research of acupuncture and moxibustion has been greatly improved, helping us gain a deeper understanding about the structure of acupoints and meridians as well as histochemical changes induced by acupuncture/moxibustion intervention. In order to promote the application of LSCM in acupuncture and moxibustion, we simply reviewed some recent studies in this field and combined them with our experience, trying to provide some technical suggestions. We expect that the technique of LSCM could be integrated into more experiments in acupuncture medicine to provide more powerful morphological evidence for exploring the underlying mechanisms of acupuncture and moxibution therapies.
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OBJECTIVE: To observe the changes of intracellular calcium ([Ca2＋]i) concentration and expression of calcium/calmodulin dependent protein kinaseⅡ (CaMKⅡ) in spinal dorsal horn neurons of spared nerve injury (SNI) rats, so as to explore its mechanisms underlying improvement of neuropathic pain. METHODS: One hundred and ten SD rats were randomly divided into 5 groups: sham control, model, EA, AP-5 and L-NAME groups. The sham group underwent only a simple separation of the sciatic nerve but without ligation and abscission. The neuropathic pain model was established by abscission of the right tibial and common peroneal nerve. EA (2 Hz, 1－3 mA) was applied to right "Weizhong" (BL 40) and "Huantiao" (GB 30) for 30 min, once a day for 7 days, starting from day 11 after surgery. For rats of the AP-5 and L-NAME groups, AP-5 (a competitive antagonist for NMDA receptor, 0.7 mg·kg－1·d－1) and L-NAME (a non-selective antagonist for nitric oxide synthase [NOS], 60 mg·kg－1·d－1) were respectively administrated by intraperitoneal injection, once daily for 7 days. The mechanical pain threshold was measured, and the calcium fluorescence intensity (shown by Fluo-3/AM calcium fluorescence indicator) of the superficial layer of the lumbar spinal cord (L 4－L 6) was measured by immunohistochemical staining and the expression of spinal cord (L 4－L 6) CaMK Ⅱ protein was detected by Western blot (WB). RESULTS: After modeling, the mechanical pain threshold was significantly decreased on day 10 and 16 after operation in comparison with the sham operation group and baseline data of pre-operation in each group (P<0.01), and remarkably increased in the EA, AP-5 and L-NAME groups relevant to the model group on day 16 (P<0.01, P<0.05), while the effect of EA was significantly superior to that of AP-5 and L-NAME groups (P<0.05), suggesting a reduction of EA analgesia after administration of AP-5 and L-NAME. The concentration of intracellular [Ca2＋]i was significantly higher in the model group than in the sham group, and considerably lower in the EA, AP-5 and L-NAME groups than in the model group (P<0.01, P<0.05). Moreover, the expression level of CaMKⅡ shown by WB and immunohistochemical staining was significantly higher in the model group than in the sham group (P<0.05) and obviously lower in the EA group (not the AP-5 and L-NAME groups) than in the model group on day 16 after the intervention (P<0.05). It suggests an involvement of glutamate NMDA receptor and NMDAR-NOS/NO signaling in the analgesic effect and CaMKⅡ expression down-regulation of EA. CONCLUSIONS: EA can ease pain in rats with neuropathic pain, which is closely related to its effect in reducing the calcium concentration and the expression of CaMKⅡ in the lumbar spinal cord, possibly mediated by glutamate NMDA receptor and NMDAR-NOS/NO signaling.
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Objective To study the protective effects of choline on myocardial ischemia rat heart and its potential mecha -nisms .Methods Ischemia hypoxia environment was simulated with low value of pH (pH 6 .8) and lack of oxygen .Calcium currents were recorded by whole cell patch under the voltage clamp configuration .The alternations in[Ca2 + ]induced by KCl was detected by laser scanning confocal microscope in ventricular myocytes ,then disccuss the effects of choline on calcium and calcium store in cells . Results The normalized peak currents of ICa-L in ventricular myocytes were larger in pH 6 .8 group than those in pH 7 .4 group , which can be attenuated by choline .The(Ca2 + )i induced by KCl in ventricular myocytes were significantly increased in pH 6 .8 Ty-rode solution and its increasing can be suppressed by choline .4-DAMP can inhibit the suppressing effect of choline .Conclusion The possible mechanism of M 3 receptor involved in the protection of ischemic myocardium by inhibiting myocardial cells in ICa-L ,in-hibiting intracellular calcium overload .
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Objective To investigate the changes in intracellular Ca2+ in the ureter smooth muscle cells (USMC) of rats with neuropathic urinary tract dysfunction (NUTD) and their significance.Methods Forty-five rats were randomly and averagely divided into NUTD group,experimental control (EC) group and blank control (BC) group.The NUTD group was operated with a spinal cord transection at the first lumbar level and the sacral cord was destroyed;in EC group the spinal process was partly bitten at the same position,but the spinal cord was not transected;BC group was given no operations.One week later,the video-urodynamic was performed to observe the acontractile detrusor (ACD),vesicoureteral reflux (VUR) and urinary tract dysfunction in rats among the NUTD group,EC group and the BC group.Video-urodynamic assessment was performed at the sixth week after operation.Ureter smooth muscle cells (USMC) were obtained by collagenase digestion.Intracellular Ca2 + in the USMC were observed by laser scanning confocal microscope.Then the effects of Bay K8644(10-8 mol/L,10-7 mol/L,10-6 mol/L) on cytosolic Ca2+ concentrations([Ca2+] i) in NUTD group were studied by calculating the fluorescence intensity.Results ACD and no detrusor overactivity were found in all rats in NUTD group and without vesicoureteral reflux.Immunofluorescence method confirmed that the cells were USMC.Compared with BC group (31.44 ± 2.82) and EC group (32.06 ± 3.67),the fluorescence intensity (FI) of intracellular Ca2 + in USMC was much lower in the NUTD group (9.80 ± 1.11),and there was significant difference(P ＜ 0.05).Bay K8644 (10-8 mol/L,10-7 mol/L,10-6 mol/L) increased the FI of [Ca2 +] i in a concentration-dependent manner,which were 3.80 ± 1.30,10.04 ± 2.15,19.89 ± 2.06,respectively,and there was significant difference (P ＜ 0.05).Conclusions The decrease in Ca2 + concentration in the ureter smooth muscle cells may be one of the important factors for the primary ureteral dysfunction of NUTD.And calcium channel agonist can be meaningful for adjusting abnormal Ca2+ concentration in USMC of NUTD.
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Objective To observe the vasodilation effect of extract of Jasminum samba (EJs), a kind of traditional Chinese medicine, on ex vivo rat thoracic aortic rings, and to investigate its mechanism. Methods On ex vivo aortic ring perfusion device, influence of EJs on contraction of the aorta induced by phenylephrine (PE) or potassium chloride (KCl) was observed. Influence of N-nitro-L-arginine-methylester ( L-NAME ), barium chloride ( BaCl2 ), glibenclamide ( Gli ) on vasodilating effect of EJs (0. 5, 1, 2, 4, 8 g·L-1 ) was detected. Effect of EJs on the contraction of calcium chloride (CaCl2 ) and PE in Ca2+-free medium was detected. [ Ca2+ ] i in vascular smooth muscle cells was determined by using laser scanning confocal microscope (LSCM). Results In blood vessels with intact endothelium, EJs concentration-dependently decreased PE- or KCl-induced vasoconstriction, the maximum dilating effect being (105. 0±3. 2)% and (78. 0±6. 5)% , respectively; L-NAME affected the vasodilatory effect of EJs on thoracic aorta rings ( P<0. 01), the maximum dilatory effect being (58. 0 ± 6. 9)% . BaCl2 and Gli had significant influence on vasodilation of EJs, and the contraction was obviously attenuated (P<0. 01), the maximum dilatory effect being (37. 0±5. 2)% and (78. 0±10. 0)% , respectively. EJs significantly inhibited contracting effect of PE on thoracic aorta rings in Ca2+-free medium (P<0. 01). The maximum contraction effect was (70. 0±6. 3)% . EJs inhibited CaCl2-induced vasoconstriction (0. 5-8 mmol·L-1 ), and vasoconstriction was decreased by (65. 0±3. 2)% . LSCM recorded that Fmax / F0 of 4 and 8 g·L-1 EJs was (2. 0±0. 2) and (1. 5±0. 2), respectively. Conclusion EJs exerted a dose-dependent vasodilating effect on rat isolated aorta rings. The mechanism might be related to promoting NO release, activating K+channels and decreasing the concentration of cytoplasmic Ca2+.
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Background Fungal corneal ulcer is a visual-threatening eye disease,and drug therapy has a limiting efficacy.Corneal transplantation or eye enucleation sometimes is necessary to the severe patients.Corneal collagen cross-linking (CXL) is an effective method for some corneal diseases,but the study on CXL for fungal corneal ulcer is lack.Objective This study was to evaluate the clinical effectiveness and safety CXL for fungal corneal ulcer.Methods Fifteen 8-week-old healthy New Zealand white rabbits were used in this study and other 5 rabbits served as normal controls.Fungal corneal ulcer models were established in the right eyes of other 10 rabbits by infecting sickle bacteria liquid after corneal scratching and removing corneal epithelium,then decellularized ostrich corneal patch covered the defected cornea.The models were randomly divided into the non-treatment group and the CXL treatment group.Corneal lesions were examined under the slit lamp microscope every day,and cornea was pictured by laser scanning confocal microscope on the 3rd,7th,14th,21st and 28th day individually after CXL.All rabbits were sacrificed and corneal tissues were obtained 4 weeks after treatment,and the collagen fiber diameter and fibrocytes were observed under the scanning electron microscope.Results Fungal corneal ulcer models were successfully established by corneal scratching and decellularized ostrich cornea covering.The gray ulcer lesions and hypbae like bean pod were seen by slit lamp microscope and laser scanning confocal microscope 3 days after modeling.Corneal ulcer deepened and expanded 1 week later,and there were a large number of spore and hyphae criss-crossing as short rod in shallow stroma.Inflammatory cells were observed in corneal endothelial cells and ocular anterior chamber.In the CXL treatment group,the range of corneal epithelial deficiency was less than that in the nontreatment group on the 3rd,7th,14th,and 21st (all at P＜ 0.05).The diameters of collagen fibers were (24.6± 1.8) nm,(24.9 ± 1.9) nm and (43.0 ± 7.4) nm in the normal control group,non-treatment group and CXL treatment group,showing a significant difference among the 3 groups (F =27.05,P =0.00),and the collagen diameters were thicker in the CXL treatment group than those in the normal control group and non-treatment group (t =5.40,-5.30,both at P＜0.05),and fibrocytes were seen among the collagen fibers.No significant difference was found in the collagen diameters between the non-treatment group and normal control group,and the fibrocytes were less in the non-treatment group.Conclusions CXL therapy can treat fungal corneal ulcer by enhancing collagen,promoting fibrocytes proliferation,suppressing fungus and inflammatory response and accelerating tissue repair.
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Objective To investigate the influence of primary cultured neonatal rat hippocampal neurons caused by human cytomegalovirus (HCMV AD169) infection on intracellular calcium and its mechanism.Methods Twenty SPF SD rats born within 24 hours(10 cases of male and 10 cases of female) were assigned to establish the primary rat hippocampal neuronal monolayer cells; After cultured 8 days in vitro,the eligible cells were randomly divided into HCMV infection group,HCMV + MK-801 group,MK-801 group and control group,with 10 wells in each group.The fluorescence intensity values of the intracellular free calcium were detected after 24 hours of treatment with Fluo-3AM fluorescence staining.Results Inoculation of HCMV neurons after 24 h turned to round and swollen gradually,and 4days later,most of the cells disappeared; by immunohistochemistry in cultures of hippocampal neurons in HCMV,visible early proteins,brownish yellow granules,hematoxylin were found after being stained with brown pigment.The fluorescence intensity values of neuronal intracellular calcium (215.5 ± 14.9) in HCMV group was higher than that of control group (116.4 ± 5.9) (t =15.2,P ＜ 0.01),whilerise,that in MK-801 group (88.1 ± 4.5) was significantly lower than that of control group,with decreased rate of (24.0 ± 6.7) ％ (t =-9.3,P ＜ 0.01).The fluorescence intensity values of neuronal intracellular calcium in HCMV + MK-801 group (135.5 ± 8.6) was significantly decreased compared with that of HCMV group (215.5 ± 14.9),with decreased rate of (37.0 ± 3.4) ％ (t =11.3,P ＜ 0.01).Conclusions Intracellular calcium overload of cultured rat hippocampal neurons in vitro with HCMV AD16 strains infection can be detected.One of its main mechanisms is the N-methyl-D-aspartic acid receptor channel-mediated calcium influx.
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@#Objective To study the intracellular calcium ([Ca2+ ]i) in myocardial cell of obesity rats induced by high-fat diet. Methods Male Sprague-Dawley (SD) rats were divided into obesity resistant (OR, n=15), normal (Nor, n=15) and obesity prone (OP, n=15) group after fed with high-fat diet for 10 weeks. Their body fat and serum lipids were measured. Myocardial cells were isolated with Langendorff perfusion and [Ca2+]i was measured with calcium indicator Fluo-3/AM and laser scanning confocal microscope after KCl depolarization and caffeine- induced. Results Compared with those in Nor and OR rats, the epididymal fat, perirenal fat, omental fat and body fat increased in OP rats (P<0.05), as well as the the level of total cholesterol, triglyceride and low density lipoprotein (P<0.05); the vary of [Ca2+]i elevation and restoration were lower (P<0.05). Conclusion The vary of [Ca2+ ]i elevation decreases in OP rats after KCl depolarization and caffeine-induced, that may associated with arrhythmia in obesity rats.
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Objective: To study the effect of apigenin on the expression of microglia in penumbra and cerebral water content after acute transient focal cerebral ischemia-reperfution injury in rats. Methods: The acute transient focal cerebral ischemia-reperfusion models in rats were established with the modified suture method. Male Sprague-Dawley rats were randomly divided into Sham group, model group, and apigenin groups (there were 6, 24, 48, 72 h, and 7 d reperfusion treatments in the model and apigenin groups, n = 12). All of them are 11 groups. The neurological behavior scores were valued. By FITC labeled isolectin B4 (FITC-ILB4) histochemistry staining, the infiltration of monocytes and the changes of cell morphology and number of brain-derived microglia in penumbra of six rats in every group were observed under laser scanning confocal microscope (LSCM). Water content was measured in isolated brain tissue of other six rats. Results: The positive cells of ILB4 (ILB4+) including microglia cells (Rhod 6G-) and infiltration of monocytes (Rhod 6G+) were found in cerebral ischemic area around penumbra of rats after 6 h ischemia-reperfusion in model group; The morphology changed to Amoeba-like; Microglia increased significantly after 48 h and reached to peak in 72 h, which mainly belonged to the proliferation of brain-derived microglia in Amoeba-like morphology. Microglia cell decreased in 7 d, and microglia in apigenin group obviously decreased more than that in model group (P<.05, 0.01) with the similar morphological change in corresponding time points. In 48 and 72 h of cerebral ischimia, the water content in brain tissue of rats in apigenin group was markedly lower than that in model (P<0.01). There was negative line correlation between the neurological behavior score and the number of ILB4 + cells in penumbra of model group (r=-0.415, P<.05). Apigenin could reduce the degree of neurological deficiency in model group and mitigate the brain injury effectively. Conclusion: A part of microglia cells inpenumbra are associated with brain injury; Apigenin shows the protection on acute transient focal cerebral ischemia-reperfution injury in rats, which maybe relates with down-regulating the microglia cell number and inhibiting the excessive activation of microglia cell.
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Objective To investigate the correlation between apolipoprotein E (protein:apoE;gene:APOE) polymorphisms and intracellular Ca2 + concentration in the early stage after astrocyte injury.Methods ( 1 ) The CDS region of three APOE alleles was obtained by using reverse transcription polymerase chain reaction (RT-PCR). Then, the recombinant plasmid pEGFP-N1-APOE was constructed and identified by sequencing. (2) Astrocytes were separated from APOE gene-knockout mice for immunocytochemical identification. The recombinant plasmid was transfected into the astrocytes with liposome-mediated method to screen the cell lines that could stably express APOE information. (3) Cell injury models were set up by scarification. Laser scanning confocal microscope (LCSM) was used to detect the dynamic changes of intracellular Ca2+ at 12, 24, 48 and 72 hours postinjury. Results Compared with the control group ( before injury ), every allele showed significant changes of fluorescence intensity of Ca2 + ( P ＜0.05). At 12 hours after injury, the fluorescence intensity of Ca2+ was weak, with no statistical difference between three groups ( P ＞ 0. 05 ). At 24,48 and 72 hours postinjury, the fluorescence intensity was increased progressively, with significant higher intensity in ε4 group than the other two groups (P ＜0.05 ). Conclusions The concentration of intracellular Ca2+ in the astrocytes carrying APOEε4 allele is higher than that of those carrying APOEε2 and ε3 alleles, indicating that APOEε4 carriers may activate Ca2+ channel and lead to aggravation and poor prognosis of acute injury.
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Here we reviewed the applications of laser scanning confocal microscope in biomedical field. The reformation and improvement based on this technique were also summarized. After analyzing the defects, we highlighted its potential applications in the future.
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Objective To investigate the relatonahip between TNF-α and ventricular arrhythmias after acute myocardial infarction(AMI)and its mechanism.Method Both the clinical and animal experiments were done.(1)Clinical experiment:Eighty patients with AMI were included in Union Hospital,Tongji Medical College,Huazhong University of Science and Techology,from May 2005 to November 2006 according to the WHO diagnostic criteria.Co-infection of diseases such as severe upper respiratory infection,lung infection,high fever,cancer,et al were excluded.The relationship between the levels of TNF-α and arrhythmias were observed at different times after AMI.A straight line correlation,analysis Was done.(2)Animal experiment:Different concentrations of TNF-αwere added to isohted rat hearts for observing the arrhythrnia effects.The effect of TNF-α on intracellular Ca2+ concentration was detected by laser confocal technique.All data were analyzed by SNK-q test using SPSS 13.0 sofeware prograrn.Results(1)The plasma levels of TNF-α were significantly associated with the Lown class of PVC after AMI and they were higher in AMI of anterior wall[(46.41±10.34)pg/ml]than other positions [(28.25±6.35)pg/ml,P<0.05].2)The frequency of ventricular arrhythmias was interrelated with the concentralions of TNF-α.Using etanercept beforehand,TNF-α induced a slight increase of intracellular Ca2+ intensity (P<0.05).Conclusions There was a relationship between TNF-αlevels and ventricular arrhythmisa in patients with AMI.Animal experiments confirmed the isolated heart perfusion with TNF-α induced ventricular arrhytrnias.Expression of TNF-α after AMI was related with the occurrence of ventricular arrhythrnias.The effect might be associated with the increased inuaeellular Ca2+ intensity caused by TNF-α.
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Objective To explore the double-labeling method of monitoring the GHRP regulatory function on [Ca2+]i and NO in cardiomyocytes of rats on real time under LSCM.Methods The reformed constant-flow Langendorff system and enzyme-dissociated was used to isolate cardiomyocytes.[Ca2+]i and NO in the cardiomyocytes of SD rats were double-labeled by their molecular probe Rhod-2/AM and DAF-FM/DA,respectively to monitor the regulatory function of GHRP on [Ca2+]i and NO on real time by LSCM.Results Ca2+ signal showed a red fluorescence and NO showed a green fluorescence while the overlapping of the two signals showed a yellow-green fluorescence by this system,and the similar effect presents in both double-labeled state and the single labeled one:GHRP induced a transient[Ca2+]i increase then followed by a plateau phase while there was not significant change in NO signal system after GHRP stimulation under the LSCM in the cardiomyocytes of rats.Conclusions After having established the double-labeling method we monitored the GHRP regulatory function on [Ca2+]i and NO on real time in cardiomyocytes of rats under LSCM causing the [Ca2+]i biphasic increase while no significant change in NO signal system.
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Aim: The purpose of this study was to observe the effect of 15-HETE on rabbit pulmonary artery (PA) vasoconstriction after removing extracellular Ca2+ and on [Ca2+]i in PASMCs and to discuss the mechanisms of cytosolic Ca2+ mobilization induced by 15-HETE. Methods: We used tention studies of PA rings to observe the effect of L-type Ca2+ channel blocker and non-Ca2+ solution on PA vasoconstriction induced by 15-HETE. Then we used laser-scanning confocal microscope to investigate [Ca2+]i signaling in cultured PASMCs. Results: L-type Ca2+ channel blocker and non-Ca2+ solution had no effect on 15-HETE induced vasoconstriction in normoxic and hypoxic rabbit PA rings. The increase of [Ca2+]i was shown in 15-HETE group cells and the change in [Ca2+]i induced by 15-HETE was significantly different from that of control. Conclusion: 15-HETE may activate Ca2+ release from intracellular stores and raise [Ca2+]i in PASMCs.
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AIM: To investigate the effects and mechanisms of swainsonine-induced apoptosis on SGC-7901 cells. METHODES: After being treated with swainsonine, effective dose and median inhibition concentration (IC50) of swainsonine to SGC-7901 cells were examined by MTT assay. Cell cycle distribution and apoptotic rates were analyzed by flow cytometry. Expression of p53, c-myc and Bcl-2 were determined by immunocyto- chemical method, and the concentration of Ca2+ intra-cellular ([Ca2+]i ) was measured by the laser scanning confocal microscope (LSCM). RESULTS: Swainsonine inhibited cell growth of SGC-7901 in vitro, IC50 of 24 h was 0.84 μg·ml-l, and complete inhibition concentration of swainsonine was 6.2 μg·ml-l. Treated with swainsonine at the concentrations of 0.5, 1.5 and 4.5 μg·ml-l for 24 h, the expression of apoptosis inhibiting gene p53 and bcl-2 decreased, and apoptotic trigger gene c-myc increased (P<0.05), as well as [Ca2+]i overloading, SGC-7901 cell was induced to apoptosis in the end. The percentage of S phase were 38.8%, 39.7% and 29.6%, respectively (20.0% in control group and 23.2% in 5-Fu group), the percentage of G2/M phase were 4.5%, 1.7% and 5.3%, respectively (5.5% in control group and 9.0% in 5-Fu group), and the percentage of G1/M phase was not altered. SGC-7901 cells were treated by swainsonine at the concentrations of 0.5, 1.5 and 4.5 μg·ml-l for 24 h. Compared with the control group, the percentage of S phase were increased and that of G2/M cells were decreased significantly in treatment groups (P<0.01). CONCLUSION: Swainsonine can inhibit the cell proliferation and induce apoptosis of SGC-7901 cells, the mechanisms of swainsonine-induced apoptosis may related with [Ca2+]i overloading and expression of apoptosis-related genes.
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0.05).Intracellular Ca2+ FI in rat ventricular myocytes induced by KCl was inhibited significantly in group B2 and B3 compared with that in group C(P
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0.05).Conclusion MSCs could derive to cardiomyocyte-like cells after induction and incubation for 4 weeks in vitro,of which Ca~(2+)/CaMKⅡ is similar to the normal cardiomyocytes cells.
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Objective To explore the functional changes of gap junctional intercellular communication(GJIC) in bladder smooth muscle. Methods The functions of GJIC in bladder smooth muscle were detected by fluorescence recovery after photobleaching(FRAP). The mean fluorescence recovery rates of the bladder smooth muscle cells in the experimental group and the control group were compared. Results The mean fluorescence recovery rate of the experimental group was significantly higher than that in the control group( P
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Aim To explore the vasodilative effect on rat thoracic aortic ring of total flavonoids of Buckwheat flowers and leaves(TFBFL) and the underlying mechanisms.Methods Isometric tension measurements were used to study the effect of TFBFL on isolated rat thoracic aorta rings.Laser scanning confocal microscope was employed to measure the concentration of intracellular free calciums.Results In aorta rings precontracted with phenylephrine or potassium chloride,TFBFL caused a dose-dependent relaxation in both endothelium-intact and denuded rings and the relaxant effect of TFBFL was more potent on endothelium-intact aorta rings than that on endotheliumdenuded aorta rings(P