通过电解水制备氢气是实现“碳中和”目标的理想途径之一.因此,可在全p H条件下使用的氢析出(HER)催化剂的研发是近年来电催化领域的研究热点.原子级分散的催化剂,能够在保留铂族金属(PGM)固有活性的同时,降低催化剂中PGM的用量.虽然可...通过电解水制备氢气是实现“碳中和”目标的理想途径之一.因此,可在全p H条件下使用的氢析出(HER)催化剂的研发是近年来电催化领域的研究热点.原子级分散的催化剂,能够在保留铂族金属(PGM)固有活性的同时,降低催化剂中PGM的用量.虽然可以通过X射线吸收光谱(XAS)来表征原子分散的PGM电催化剂的配位环境,但目前对原子空间分布的控制仍然具有挑战.本文制备了钒掺杂钨青铜内通道氨配位的钌单原子催化剂(Ru/V-NHWO),用于全p H范围内的HER反应.采用X射线衍射(XRD)、高角环形暗场扫描透射电镜(HAADF-STEM)、X射线光电子能谱(XPS)和原位X射线吸收光谱(XAS)等进行表征,研究了钌单原子与V-NHWO载体的结合方式以及构效关系,并采用密度泛函理论(DFT)计算探索了催化剂中诸多位点的活性贡献.在1 mol/LKOH, 0.5 mol/L H_(2)SO_(4)和1 mol/L磷酸盐缓冲溶液中,其在10 m Acm^(-2)下的过电位分别为28.0, 29.6和40.6 m V.同时,在过电位100 m V时,质量活性分别达到3930, 1941和602.8 m Amg^(-1)Ru,数倍于同等条件下的商业铂碳.XRD结果表明,钌的引入可以确保催化剂在氩气条件下热解后仍保持六方钨铵青铜晶相,证明钌与钨铵青铜六方晶体通道内氨物种,即“通道氨”的结合.HAADF-STEM结果表明,钌原子与NHWO间存在强烈相互作用,有助于提升HER性能.XPS和XAS结果表明, W5+信号出现在引入钌后,峰位置的结合能增加且峰面积降低,说明钌与通道氨之间存在相互作用.N的XPS结果表明,钌的引入导致了金属氨键的形成.XAS结果表明, Ru/V-NHWO/CC中钌单原子和钌团簇共存,钌单原子与通道氨配位,并且钒的引入会诱发V-NHWO中金属键长缩短,这表明催化剂的金属性得到了提升,有利于改善其导电性.采用DFT计算进一步研究了HER活性的来源.相比于V-NHWO载体和钌团簇修饰的V-NHWO,以单原子形式结合的钌具有更低的水解离能垒,该能垒在氨桥接的钌双原子垂直插入、钒掺杂和多通道插入等多种因素作用下进一步降低.同时,氢中间体结合能得到了相应的优化而趋近于0 e V.此外,差分电荷密度模拟结果表明,氢中间体结合后, V-NHWO对于钌单原子存在明显的供电子行为,有利于HER动力学过程.综上,本工作报道了金属载体对于高分散金属原子空间分布调控的重要作用,可为设计和构筑可应用于诸多能源转换过程的新型原子级分散催化剂提供参考.展开更多
Vacuum ultraviolet photon-induced ionization and dissociation of isoleucine are investi- gated with synchrotron radiation photoionization mass spectroscopy and theoretical cal- culations. The main fragment ions at m/z...Vacuum ultraviolet photon-induced ionization and dissociation of isoleucine are investi- gated with synchrotron radiation photoionization mass spectroscopy and theoretical cal- culations. The main fragment ions at m/z=86, 75, 74, 69, 57, 46, 45, 44, 41, 30, 28, and 18 from isoleucine are observed in the mass spectrum at the photon energy of 13 eV. From the photoionization efficiency curves, appearance energies for the principal fragment ions CsH12N＋ （rn/z=86）, C2H5NO2＋ （m/z=75）, C5H9＋ （rn/z=-69）, C4H9＋ （m/z=57）, and CH4N＋ （m/z=30） are determined to be 8.844-0.07, 9.254-0.06, 10.20-4-0.12, 9.254-0.10, and 11.05＋0.07 eV, respectively, and possible formation pathways are established in detail by the calculations at the B3LYP/6-31＋＋G（d, p） levels. These proposed channels include simple bond cleavage reactions as well as reactions involving intermediates and transition structures. The experimental and computational appearance energies or barriers are in good agreement.展开更多
Aim To determine the effects of glucose on APD, I_(K1) , I_K , I_(Ca-L), ofventricular myocytes in guinea pigs, Methods Whole-cell patch-clamp technique was used to record thechanged action potential ionic current ind...Aim To determine the effects of glucose on APD, I_(K1) , I_K , I_(Ca-L), ofventricular myocytes in guinea pigs, Methods Whole-cell patch-clamp technique was used to record thechanged action potential ionic current induced by glucose of single cell in guinea pig ventricularmyocytes, to compare the action of 0, 10 and 20 mmol·L^(-1) glucoses on trans-membrane ioniccurrent. Results (1) Compared with 10 mmol·L^(-1) glucose concentrations, 0 and 20 mmol·L^(-1)glucose both shortened APD of ventricular myocytes ( P < 0.05). (2) The inward components ofI_(K1) density were maximal when the glucose concentration was at 10 mmol·L^(-1) . Normalized Ⅰ -Ⅴ relationships showed that both 0 and 20 mmol·L^(-1) glucose produced a left-shift of Ⅰ - Ⅴcurve. The reverse potential changed from - 72.4 mV to - 64.6 mV. (3) Compared with 10 mmol·L^(-1),both 0 and 20 mmol·L^(-1) glucose markedly increased the I_(Ca-L) amplitude and density. TheI_(Ca-L) current density was ( - 8.035 +- 0.82) pA/pF ( n = 8) at a test potential of 10 mV when theglucose concentration was 10 mmol·L^(-1) . But its current density decreased to ( - 5.45 +- 0.67)pA/pF and ( - 6.50 +- 0.56) pA/pF when glucose concentrations were 0 and 20 mmol·L^(-1) ,respectively. (4) The current densities of I_K were (18.96+-2.86) pA/pF, (8.66 +-1.87) pA/pF, and(15.32 +- 3.12) pA/pF, at + 70 mV for 0, 10 and 20 mmol·L^(-1) glucoses, respectively. ConclusionGlucose in different concentrations has different effects on APD, I_(K1), I_K, and I_(Ca-L) ofsingle ventricular myocyte in guinea pigs. There are similar actions of 0 and 20 mmol· L^(-1)glucoses on the transmembrane ionic current of ventricular myocytes in guinea pigs.展开更多
The acrosome reaction （AR）, an absolute requirement for spermatozoa and egg fusion, requires the influx of Ca2＋ into the spermatozoa through voltage-dependent Ca2＋ channels and store-operated channels. Maitotoxin ...The acrosome reaction （AR）, an absolute requirement for spermatozoa and egg fusion, requires the influx of Ca2＋ into the spermatozoa through voltage-dependent Ca2＋ channels and store-operated channels. Maitotoxin （MTx）, a Ca2＋-mobilizing agent, has been shown to be a potent inducer of the mouse sperm AR, with a pharmacology similar to that of the zona pellucida （ZP）, possibly suggesting a common pathway for both inducers. Using recombinant human ZP3 （rhZP3）, mouse ZP and two MTx channel blockers （U73122 and U73343）, we investigated and compared the MTx- and ZP-induced ARs in human and mouse spermatozoa. Herein, we report that MTx induced AR and elevated intracellular Ca2＋ （[Ca2＋]~） in human spermatozoa, both of which were blocked by U73122 and U73343. These two compounds also inhibited the MTx-induced AR in mouse spermatozoa. In disagreement with our previous proposal, the AR triggered by rhZP3 or mouse ZP was not blocked by U73343, indicating that in human and mouse spermatozoa, the AR induction by the physiological ligands or by MTx occurred through distinct pathways. U73122, but not U73343 （inactive analogue）, can block phospholipase C （PLC）. Another PLC inhibitor, edelfosine, also blocked the rhZP3- and ZP-induced ARs. These findings confirmed the participation of a PLC-dependent signalling pathway in human and mouse zona protein-induced AR. Notably, edelfosine also inhibited the MTx-induced mouse sperm AR but not that of the human, suggesting that toxin-induced AR is PLC-dependent in mice and PLC-independent in humans.展开更多
Most axons in the vertebral central nervous system are myelinated by oligodendrocytes.Myelin protects and insulates neuronal processes,enabling the fast,saltatory conduction unique to myelinated axons.Myelin disruptio...Most axons in the vertebral central nervous system are myelinated by oligodendrocytes.Myelin protects and insulates neuronal processes,enabling the fast,saltatory conduction unique to myelinated axons.Myelin disruption resulting from trauma and biochemical reaction is a common pathological event in spinal cord injury and chronic neurodegenerative diseases.Myelin damage-induced axonal conduction block is considered to be a significant contributor to the devastating neurological deficits resulting from trauma and illness.Potassium channels are believed to play an important role in axonal conduction failure in spinal cord injury and multiple sclerosis.Myelin damage has been shown to unmask potassium channels,creating aberrant potassium currents that inhibit conduction.Potassium channel blockade reduces this ionic leakage and improves conduction.The present review was mainly focused on the development of this technique of restoring axonal conduction and neurological function of demyelinated axons.The drug 4-aminopyridine has recently shown clinical success in treating multiple sclerosis symptoms.Further translational research has also identified several novel potassium channel blockers that may prove effective in restoring axonal conduction.展开更多
TRPP2 channel protein belongs to the superfamily of transient receptor potential(TRP) channels and is widely expressed in various tissues, including smooth muscle in digestive gut. Accumulating evidence has demonstrat...TRPP2 channel protein belongs to the superfamily of transient receptor potential(TRP) channels and is widely expressed in various tissues, including smooth muscle in digestive gut. Accumulating evidence has demonstrated that TRPP2 can mediate Ca^(2+) release from Ca^(2+) stores. However, the functional role of TRPP2 in gallbladder smooth muscle contraction still remains unclear. In this study, we used Ca^(2+) imaging and tension measurements to test agonist-induced intracellular Ca^(2+) concentration increase and smooth muscle contraction of guinea pig gallbladder, respectively. When TRPP2 protein was knocked down in gallbladder muscle strips from guinea pig, carbachol(CCh)-evoked Ca^(2+) release and extracellular Ca^(2+) influx were reduced significantly, and gallbladder contractions induced by endothelin 1 and cholecystokinin were suppressed markedly as well. CCh-induced gallbladder contraction was markedly suppressed by pretreatment with U73122, which inhibits phospholipase C to terminate inositol 1,4,5-trisphosphate receptor(IP3) production, and 2-aminoethoxydiphenyl borate(2APB), which inhibits IP3 recepor(IP3R) to abolish IP3R-mediated Ca^(2+) release. To confirm the role of Ca^(2+) release in CCh-induced gallbladder contraction, we used thapsigargin(TG)-to deplete Ca^(2+) stores via inhibiting sarco/endoplasmic reticulum Ca^(2+)-ATPase and eliminate the role of store-operated Ca^(2+) entry on the CCh-induced gallbladder contraction. Preincubation with 2 μmol L^(-1) TG significantly decreased the CCh-induced gallbladder contraction. In addition, pretreatments with U73122, 2APB or TG abolished the difference of the CCh-induced gallbladder contraction between TRPP2 knockdown and control groups. We conclude that TRPP2 mediates Ca^(2+) release from intracellular Ca^(2+) stores, and has an essential role in agonist-induced gallbladder muscle contraction.展开更多
In the present study,we aimed to investigate the effect of puromycin aminonucleoside(PAN)on the expression and distribution of transient receptor potential canonical 6(TRPC6)of murine podocytes and further study the p...In the present study,we aimed to investigate the effect of puromycin aminonucleoside(PAN)on the expression and distribution of transient receptor potential canonical 6(TRPC6)of murine podocytes and further study the protective mechanism of fluvastatin on podocyte injury by TRPC6 in vitro.Podocytes were treated by PAN at different doses and at different time points.The expressions of TRPC6 at mRNA and protein levels were assessed.An immunofluorescent assay was used to observe the distribution of TRPC6.Cultured podocytes were then divided into four groups.The expressions of TRPC6 at mRNA and protein levels were measured.The intracellular calcium concentration of podocytes was measured with a laser-scanning confocal microscope.The paracellular permeability to BSA was evaluated using Millicell-PCF Inserts.The expressions of TRPC6 at mRNA and protein levels were increased in a dose and time-dependent manner after exposure to PAN.Immunofluorescence showed that the expression intensity of TRPC6 was significantly increased,and the distribution of TRPC6 was changed after PAN was applied to podocytes.With fluvastatin intervention,PAN-induced up-regulation of TRPC6 was significantly reversed.The ratio of the peak value of intracellular calcium to the basic calcium value in the PAN group was significantly higher after TRPC6 was activated by OAG,while it is obviously reversed under the action of fluvastatin.The podocyte permeability was significantly increased after 48 h of PAN treatment,while the above situation was effectively improved after fluvastatin intervention.The changes of distribution and expression of TRPC6 were related to podocyte injury induced by PAN.Fluvastatin could exert its protective effects on podocytes by down-regulating TRPC6.展开更多
文摘通过电解水制备氢气是实现“碳中和”目标的理想途径之一.因此,可在全p H条件下使用的氢析出(HER)催化剂的研发是近年来电催化领域的研究热点.原子级分散的催化剂,能够在保留铂族金属(PGM)固有活性的同时,降低催化剂中PGM的用量.虽然可以通过X射线吸收光谱(XAS)来表征原子分散的PGM电催化剂的配位环境,但目前对原子空间分布的控制仍然具有挑战.本文制备了钒掺杂钨青铜内通道氨配位的钌单原子催化剂(Ru/V-NHWO),用于全p H范围内的HER反应.采用X射线衍射(XRD)、高角环形暗场扫描透射电镜(HAADF-STEM)、X射线光电子能谱(XPS)和原位X射线吸收光谱(XAS)等进行表征,研究了钌单原子与V-NHWO载体的结合方式以及构效关系,并采用密度泛函理论(DFT)计算探索了催化剂中诸多位点的活性贡献.在1 mol/LKOH, 0.5 mol/L H_(2)SO_(4)和1 mol/L磷酸盐缓冲溶液中,其在10 m Acm^(-2)下的过电位分别为28.0, 29.6和40.6 m V.同时,在过电位100 m V时,质量活性分别达到3930, 1941和602.8 m Amg^(-1)Ru,数倍于同等条件下的商业铂碳.XRD结果表明,钌的引入可以确保催化剂在氩气条件下热解后仍保持六方钨铵青铜晶相,证明钌与钨铵青铜六方晶体通道内氨物种,即“通道氨”的结合.HAADF-STEM结果表明,钌原子与NHWO间存在强烈相互作用,有助于提升HER性能.XPS和XAS结果表明, W5+信号出现在引入钌后,峰位置的结合能增加且峰面积降低,说明钌与通道氨之间存在相互作用.N的XPS结果表明,钌的引入导致了金属氨键的形成.XAS结果表明, Ru/V-NHWO/CC中钌单原子和钌团簇共存,钌单原子与通道氨配位,并且钒的引入会诱发V-NHWO中金属键长缩短,这表明催化剂的金属性得到了提升,有利于改善其导电性.采用DFT计算进一步研究了HER活性的来源.相比于V-NHWO载体和钌团簇修饰的V-NHWO,以单原子形式结合的钌具有更低的水解离能垒,该能垒在氨桥接的钌双原子垂直插入、钒掺杂和多通道插入等多种因素作用下进一步降低.同时,氢中间体结合能得到了相应的优化而趋近于0 e V.此外,差分电荷密度模拟结果表明,氢中间体结合后, V-NHWO对于钌单原子存在明显的供电子行为,有利于HER动力学过程.综上,本工作报道了金属载体对于高分散金属原子空间分布调控的重要作用,可为设计和构筑可应用于诸多能源转换过程的新型原子级分散催化剂提供参考.
基金V. ACKNOWLEDGMENTS This work is supported by the National Natural Science Foundation of China （No.10875126 and No.10979048） and the Specialized Research Fund for the Doctoral Program of Higher Education, SRF for ROCS, SEM.
文摘Vacuum ultraviolet photon-induced ionization and dissociation of isoleucine are investi- gated with synchrotron radiation photoionization mass spectroscopy and theoretical cal- culations. The main fragment ions at m/z=86, 75, 74, 69, 57, 46, 45, 44, 41, 30, 28, and 18 from isoleucine are observed in the mass spectrum at the photon energy of 13 eV. From the photoionization efficiency curves, appearance energies for the principal fragment ions CsH12N＋ （rn/z=86）, C2H5NO2＋ （m/z=75）, C5H9＋ （rn/z=-69）, C4H9＋ （m/z=57）, and CH4N＋ （m/z=30） are determined to be 8.844-0.07, 9.254-0.06, 10.20-4-0.12, 9.254-0.10, and 11.05＋0.07 eV, respectively, and possible formation pathways are established in detail by the calculations at the B3LYP/6-31＋＋G（d, p） levels. These proposed channels include simple bond cleavage reactions as well as reactions involving intermediates and transition structures. The experimental and computational appearance energies or barriers are in good agreement.
文摘Aim To determine the effects of glucose on APD, I_(K1) , I_K , I_(Ca-L), ofventricular myocytes in guinea pigs, Methods Whole-cell patch-clamp technique was used to record thechanged action potential ionic current induced by glucose of single cell in guinea pig ventricularmyocytes, to compare the action of 0, 10 and 20 mmol·L^(-1) glucoses on trans-membrane ioniccurrent. Results (1) Compared with 10 mmol·L^(-1) glucose concentrations, 0 and 20 mmol·L^(-1)glucose both shortened APD of ventricular myocytes ( P < 0.05). (2) The inward components ofI_(K1) density were maximal when the glucose concentration was at 10 mmol·L^(-1) . Normalized Ⅰ -Ⅴ relationships showed that both 0 and 20 mmol·L^(-1) glucose produced a left-shift of Ⅰ - Ⅴcurve. The reverse potential changed from - 72.4 mV to - 64.6 mV. (3) Compared with 10 mmol·L^(-1),both 0 and 20 mmol·L^(-1) glucose markedly increased the I_(Ca-L) amplitude and density. TheI_(Ca-L) current density was ( - 8.035 +- 0.82) pA/pF ( n = 8) at a test potential of 10 mV when theglucose concentration was 10 mmol·L^(-1) . But its current density decreased to ( - 5.45 +- 0.67)pA/pF and ( - 6.50 +- 0.56) pA/pF when glucose concentrations were 0 and 20 mmol·L^(-1) ,respectively. (4) The current densities of I_K were (18.96+-2.86) pA/pF, (8.66 +-1.87) pA/pF, and(15.32 +- 3.12) pA/pF, at + 70 mV for 0, 10 and 20 mmol·L^(-1) glucoses, respectively. ConclusionGlucose in different concentrations has different effects on APD, I_(K1), I_K, and I_(Ca-L) ofsingle ventricular myocyte in guinea pigs. There are similar actions of 0 and 20 mmol· L^(-1)glucoses on the transmembrane ionic current of ventricular myocytes in guinea pigs.
文摘The acrosome reaction （AR）, an absolute requirement for spermatozoa and egg fusion, requires the influx of Ca2＋ into the spermatozoa through voltage-dependent Ca2＋ channels and store-operated channels. Maitotoxin （MTx）, a Ca2＋-mobilizing agent, has been shown to be a potent inducer of the mouse sperm AR, with a pharmacology similar to that of the zona pellucida （ZP）, possibly suggesting a common pathway for both inducers. Using recombinant human ZP3 （rhZP3）, mouse ZP and two MTx channel blockers （U73122 and U73343）, we investigated and compared the MTx- and ZP-induced ARs in human and mouse spermatozoa. Herein, we report that MTx induced AR and elevated intracellular Ca2＋ （[Ca2＋]~） in human spermatozoa, both of which were blocked by U73122 and U73343. These two compounds also inhibited the MTx-induced AR in mouse spermatozoa. In disagreement with our previous proposal, the AR triggered by rhZP3 or mouse ZP was not blocked by U73343, indicating that in human and mouse spermatozoa, the AR induction by the physiological ligands or by MTx occurred through distinct pathways. U73122, but not U73343 （inactive analogue）, can block phospholipase C （PLC）. Another PLC inhibitor, edelfosine, also blocked the rhZP3- and ZP-induced ARs. These findings confirmed the participation of a PLC-dependent signalling pathway in human and mouse zona protein-induced AR. Notably, edelfosine also inhibited the MTx-induced mouse sperm AR but not that of the human, suggesting that toxin-induced AR is PLC-dependent in mice and PLC-independent in humans.
基金supported by the Purdue Research Foundation(No. 61133)National Institute of Health,USA(No.1R21 NS050174-01A1)
文摘Most axons in the vertebral central nervous system are myelinated by oligodendrocytes.Myelin protects and insulates neuronal processes,enabling the fast,saltatory conduction unique to myelinated axons.Myelin disruption resulting from trauma and biochemical reaction is a common pathological event in spinal cord injury and chronic neurodegenerative diseases.Myelin damage-induced axonal conduction block is considered to be a significant contributor to the devastating neurological deficits resulting from trauma and illness.Potassium channels are believed to play an important role in axonal conduction failure in spinal cord injury and multiple sclerosis.Myelin damage has been shown to unmask potassium channels,creating aberrant potassium currents that inhibit conduction.Potassium channel blockade reduces this ionic leakage and improves conduction.The present review was mainly focused on the development of this technique of restoring axonal conduction and neurological function of demyelinated axons.The drug 4-aminopyridine has recently shown clinical success in treating multiple sclerosis symptoms.Further translational research has also identified several novel potassium channel blockers that may prove effective in restoring axonal conduction.
基金supported by Anhui Provincial Natural Science Foundation (1208085MH181, 1108085J11)National Natural Science Foundation of China (81371284)Young Prominent Investigator Supporting Program from Anhui Medical University and National Training Program of Innovation and Entrepreneurship for Undergraduates (201310366012)
文摘TRPP2 channel protein belongs to the superfamily of transient receptor potential(TRP) channels and is widely expressed in various tissues, including smooth muscle in digestive gut. Accumulating evidence has demonstrated that TRPP2 can mediate Ca^(2+) release from Ca^(2+) stores. However, the functional role of TRPP2 in gallbladder smooth muscle contraction still remains unclear. In this study, we used Ca^(2+) imaging and tension measurements to test agonist-induced intracellular Ca^(2+) concentration increase and smooth muscle contraction of guinea pig gallbladder, respectively. When TRPP2 protein was knocked down in gallbladder muscle strips from guinea pig, carbachol(CCh)-evoked Ca^(2+) release and extracellular Ca^(2+) influx were reduced significantly, and gallbladder contractions induced by endothelin 1 and cholecystokinin were suppressed markedly as well. CCh-induced gallbladder contraction was markedly suppressed by pretreatment with U73122, which inhibits phospholipase C to terminate inositol 1,4,5-trisphosphate receptor(IP3) production, and 2-aminoethoxydiphenyl borate(2APB), which inhibits IP3 recepor(IP3R) to abolish IP3R-mediated Ca^(2+) release. To confirm the role of Ca^(2+) release in CCh-induced gallbladder contraction, we used thapsigargin(TG)-to deplete Ca^(2+) stores via inhibiting sarco/endoplasmic reticulum Ca^(2+)-ATPase and eliminate the role of store-operated Ca^(2+) entry on the CCh-induced gallbladder contraction. Preincubation with 2 μmol L^(-1) TG significantly decreased the CCh-induced gallbladder contraction. In addition, pretreatments with U73122, 2APB or TG abolished the difference of the CCh-induced gallbladder contraction between TRPP2 knockdown and control groups. We conclude that TRPP2 mediates Ca^(2+) release from intracellular Ca^(2+) stores, and has an essential role in agonist-induced gallbladder muscle contraction.
基金National Natural Science Foundation of China(Grant No.81400333)。
文摘In the present study,we aimed to investigate the effect of puromycin aminonucleoside(PAN)on the expression and distribution of transient receptor potential canonical 6(TRPC6)of murine podocytes and further study the protective mechanism of fluvastatin on podocyte injury by TRPC6 in vitro.Podocytes were treated by PAN at different doses and at different time points.The expressions of TRPC6 at mRNA and protein levels were assessed.An immunofluorescent assay was used to observe the distribution of TRPC6.Cultured podocytes were then divided into four groups.The expressions of TRPC6 at mRNA and protein levels were measured.The intracellular calcium concentration of podocytes was measured with a laser-scanning confocal microscope.The paracellular permeability to BSA was evaluated using Millicell-PCF Inserts.The expressions of TRPC6 at mRNA and protein levels were increased in a dose and time-dependent manner after exposure to PAN.Immunofluorescence showed that the expression intensity of TRPC6 was significantly increased,and the distribution of TRPC6 was changed after PAN was applied to podocytes.With fluvastatin intervention,PAN-induced up-regulation of TRPC6 was significantly reversed.The ratio of the peak value of intracellular calcium to the basic calcium value in the PAN group was significantly higher after TRPC6 was activated by OAG,while it is obviously reversed under the action of fluvastatin.The podocyte permeability was significantly increased after 48 h of PAN treatment,while the above situation was effectively improved after fluvastatin intervention.The changes of distribution and expression of TRPC6 were related to podocyte injury induced by PAN.Fluvastatin could exert its protective effects on podocytes by down-regulating TRPC6.
