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Genmed Inc ca 2+ determination kit
Taurolidine inhibits intracellular calcium release by influenza virus infection. ( A , B ) The intracellular Ca 2+ concentration was measured after VSMCs cells were infected IAV/H1N1 and IBV/S9-MD, respectively. ( C ) The Ca 2+ intensity in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( D ) Quantitative analysis of the relative calcium intensity of each group as in C . ( E ) The Ca 2+ signaling in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( F ) Quantitative analysis of the relative calcium intensity of each group as in E . ( G ) Western blotting results of p-MLC and MLC in VSMCs after IAV/H1N1 infection. ( H ) Western blotting results of p-MLC and MLC in VSMCs after IBV/S9-MD infection
Ca 2+ Determination Kit, supplied by Genmed Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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1) Product Images from "Taurolidine inhibits influenza virus infection and prevents influenza-induced cytokine storm, vasoconstriction and lung damage"

Article Title: Taurolidine inhibits influenza virus infection and prevents influenza-induced cytokine storm, vasoconstriction and lung damage

Journal: Cellular and Molecular Life Sciences: CMLS

doi: 10.1007/s00018-025-05636-6

Taurolidine inhibits intracellular calcium release by influenza virus infection. ( A , B ) The intracellular Ca 2+ concentration was measured after VSMCs cells were infected IAV/H1N1 and IBV/S9-MD, respectively. ( C ) The Ca 2+ intensity in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( D ) Quantitative analysis of the relative calcium intensity of each group as in C . ( E ) The Ca 2+ signaling in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( F ) Quantitative analysis of the relative calcium intensity of each group as in E . ( G ) Western blotting results of p-MLC and MLC in VSMCs after IAV/H1N1 infection. ( H ) Western blotting results of p-MLC and MLC in VSMCs after IBV/S9-MD infection
Figure Legend Snippet: Taurolidine inhibits intracellular calcium release by influenza virus infection. ( A , B ) The intracellular Ca 2+ concentration was measured after VSMCs cells were infected IAV/H1N1 and IBV/S9-MD, respectively. ( C ) The Ca 2+ intensity in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( D ) Quantitative analysis of the relative calcium intensity of each group as in C . ( E ) The Ca 2+ signaling in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( F ) Quantitative analysis of the relative calcium intensity of each group as in E . ( G ) Western blotting results of p-MLC and MLC in VSMCs after IAV/H1N1 infection. ( H ) Western blotting results of p-MLC and MLC in VSMCs after IBV/S9-MD infection

Techniques Used: Virus, Infection, Concentration Assay, Western Blot

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Article Snippet: Mitochondria and cytoplasmic fractions were isolated from the temporal lobes using the Mitochondria Isolation Kit for Tissue (Beyotime, China). .. Next, the Ca 2+ in cytoplasm and mitochondria were, respectively, detected by the Cytoplasmic Ca 2+ Concentration Quantitative Determination Kit (Genmed, USA) and the Mitochondrial Ca 2+ Concentration Quantitative Determination Kit (Genmed, USA). ..

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Article Title: Role of mitochondrial calcium uniporter‐mediated Ca 2+ and iron accumulation in traumatic brain injury
Article Snippet: The mitochondrial and cellular Ca 2+ concentrations were measured by Fura‐3‐AM with a mitochondrial Ca 2+ concentration quantitative determination kit (Genmed Scientifics Inc, USA, catalogue number: GMS10153) and a cellular Ca 2+ concentration quantitative determination kit (Genmed Scientifics Inc, USA, catalogue number: GMS10152).

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Article Snippet: The intracellular Ca 2+ level in basal cortex was measured with a tissue Ca 2+ concentration quantitative determination kit (GMS10157.2, Genmed Scientifics, Shanghai, China).



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Genmed Inc ca 2+ determination kit
Taurolidine inhibits intracellular calcium release by influenza virus infection. ( A , B ) The intracellular Ca 2+ concentration was measured after VSMCs cells were infected IAV/H1N1 and IBV/S9-MD, respectively. ( C ) The Ca 2+ intensity in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( D ) Quantitative analysis of the relative calcium intensity of each group as in C . ( E ) The Ca 2+ signaling in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( F ) Quantitative analysis of the relative calcium intensity of each group as in E . ( G ) Western blotting results of p-MLC and MLC in VSMCs after IAV/H1N1 infection. ( H ) Western blotting results of p-MLC and MLC in VSMCs after IBV/S9-MD infection
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Effect of EGT on intracellular Ca 2+ concentration ([Ca 2+ ] i ) in NE-4C nerve cells. (A) Real-time change of intracellular fluorescence signals with time in NE-4C nerve cells. The stimulation of EGT (1, 10, and 100 μM) started after 30 s of monitoring basal fluorescence intensity. (B) Transient changes of fluorescence from Fluo-4 after stimulation of EGT (1, 10, and 100 μM) in NE-4C nerve cells. Calcium kit II—Fluo 4 was used in this study. Transient changes in [Ca 2+ ] i [relative fluorescence units ,(RFU)] were calculated as the difference between peak ( F max ) and basal ( F 0 ) fluorescence intensity (Δ F = F max – F 0 ) at excitation wavelength of 485 nm, emission wavelength of 525 nm, and cutoff filter of 515 nm. RFU, relative fluorescence units. Values are expressed as the mean ± SD ( n = 3 or 4). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s t -test. * p < 0.05, **** p < 0.0001 vs control.
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Effect of EGT on intracellular Ca 2+ concentration ([Ca 2+ ] i ) in NE-4C nerve cells. (A) Real-time change of intracellular fluorescence signals with time in NE-4C nerve cells. The stimulation of EGT (1, 10, and 100 μM) started after 30 s of monitoring basal fluorescence intensity. (B) Transient changes of fluorescence from Fluo-4 after stimulation of EGT (1, 10, and 100 μM) in NE-4C nerve cells. Calcium kit II—Fluo 4 was used in this study. Transient changes in [Ca 2+ ] i [relative fluorescence units ,(RFU)] were calculated as the difference between peak ( F max ) and basal ( F 0 ) fluorescence intensity (Δ F = F max – F 0 ) at excitation wavelength of 485 nm, emission wavelength of 525 nm, and cutoff filter of 515 nm. RFU, relative fluorescence units. Values are expressed as the mean ± SD ( n = 3 or 4). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s t -test. * p < 0.05, **** p < 0.0001 vs control.
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Effect of EGT on intracellular Ca 2+ concentration ([Ca 2+ ] i ) in NE-4C nerve cells. (A) Real-time change of intracellular fluorescence signals with time in NE-4C nerve cells. The stimulation of EGT (1, 10, and 100 μM) started after 30 s of monitoring basal fluorescence intensity. (B) Transient changes of fluorescence from Fluo-4 after stimulation of EGT (1, 10, and 100 μM) in NE-4C nerve cells. Calcium kit II—Fluo 4 was used in this study. Transient changes in [Ca 2+ ] i [relative fluorescence units ,(RFU)] were calculated as the difference between peak ( F max ) and basal ( F 0 ) fluorescence intensity (Δ F = F max – F 0 ) at excitation wavelength of 485 nm, emission wavelength of 525 nm, and cutoff filter of 515 nm. RFU, relative fluorescence units. Values are expressed as the mean ± SD ( n = 3 or 4). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s t -test. * p < 0.05, **** p < 0.0001 vs control.
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Administration of ruthenium red (RR) or Sper protected mice against secondary brain injury and decreased Ca 2+ concentrations after traumatic brain injury (TBI). (A, B, C) Mice were subjected to TBI and then received 1 mg/kg, 3 mg/kg, 5 mg/kg of RR or 2 mg/kg, 5 mg/kg, 10 mg/kg of Sper ip injection or vehicle 30 min after TBI. NSS and Grip test score were evaluated at 1, 3 and 7 days after TBI while brain water content was examined at 1 day after TBI. (A, B) All doses of RR or Sper had an improved motor performance within 3 days; however, larger doses such as 5 mg/kg of RR and 10 mg/kg of Sper did not exhibit a better neuroprotection. This effect was no longer significant at 7 days after TBI, n = 6 per group. (C) Mice subjected to TBI or treated with vehicle had an increased brain water content as compared with the sham group. Brain water content was significantly lower in the groups treated with RR or Sper than the vehicle‐treated group. Moreover, doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect in relieving brain oedema, n = 6 each group. (D) TBI‐induced profound tissue loss of the brain was reversed by RR or Sper, and doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect. (E, F) RR or Sper treatment decreased Ca 2+ concentration following TBI. Restored cellular (E) and mitochondrial (F) concentrations of Ca 2+ by RR (3 mg/kg) or Sper (5 mg/kg) treatment after TBI, n = 6 each group. Data are presented as mean ± SEM; ** P < 0.01, *** P < 0.001 vs sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs TBI + vehicle group. Scale bar: 50 μm
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Administration of ruthenium red (RR) or Sper protected mice against secondary brain injury and decreased Ca 2+ concentrations after traumatic brain injury (TBI). (A, B, C) Mice were subjected to TBI and then received 1 mg/kg, 3 mg/kg, 5 mg/kg of RR or 2 mg/kg, 5 mg/kg, 10 mg/kg of Sper ip injection or vehicle 30 min after TBI. NSS and Grip test score were evaluated at 1, 3 and 7 days after TBI while brain water content was examined at 1 day after TBI. (A, B) All doses of RR or Sper had an improved motor performance within 3 days; however, larger doses such as 5 mg/kg of RR and 10 mg/kg of Sper did not exhibit a better neuroprotection. This effect was no longer significant at 7 days after TBI, n = 6 per group. (C) Mice subjected to TBI or treated with vehicle had an increased brain water content as compared with the sham group. Brain water content was significantly lower in the groups treated with RR or Sper than the vehicle‐treated group. Moreover, doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect in relieving brain oedema, n = 6 each group. (D) TBI‐induced profound tissue loss of the brain was reversed by RR or Sper, and doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect. (E, F) RR or Sper treatment decreased Ca 2+ concentration following TBI. Restored cellular (E) and mitochondrial (F) concentrations of Ca 2+ by RR (3 mg/kg) or Sper (5 mg/kg) treatment after TBI, n = 6 each group. Data are presented as mean ± SEM; ** P < 0.01, *** P < 0.001 vs sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs TBI + vehicle group. Scale bar: 50 μm
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Administration of ruthenium red (RR) or Sper protected mice against secondary brain injury and decreased Ca 2+ concentrations after traumatic brain injury (TBI). (A, B, C) Mice were subjected to TBI and then received 1 mg/kg, 3 mg/kg, 5 mg/kg of RR or 2 mg/kg, 5 mg/kg, 10 mg/kg of Sper ip injection or vehicle 30 min after TBI. NSS and Grip test score were evaluated at 1, 3 and 7 days after TBI while brain water content was examined at 1 day after TBI. (A, B) All doses of RR or Sper had an improved motor performance within 3 days; however, larger doses such as 5 mg/kg of RR and 10 mg/kg of Sper did not exhibit a better neuroprotection. This effect was no longer significant at 7 days after TBI, n = 6 per group. (C) Mice subjected to TBI or treated with vehicle had an increased brain water content as compared with the sham group. Brain water content was significantly lower in the groups treated with RR or Sper than the vehicle‐treated group. Moreover, doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect in relieving brain oedema, n = 6 each group. (D) TBI‐induced profound tissue loss of the brain was reversed by RR or Sper, and doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect. (E, F) RR or Sper treatment decreased Ca 2+ concentration following TBI. Restored cellular (E) and mitochondrial (F) concentrations of Ca 2+ by RR (3 mg/kg) or Sper (5 mg/kg) treatment after TBI, n = 6 each group. Data are presented as mean ± SEM; ** P < 0.01, *** P < 0.001 vs sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs TBI + vehicle group. Scale bar: 50 μm
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Ca 2+ concentration in the cytoplasm and mitochondria.
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Taurolidine inhibits intracellular calcium release by influenza virus infection. ( A , B ) The intracellular Ca 2+ concentration was measured after VSMCs cells were infected IAV/H1N1 and IBV/S9-MD, respectively. ( C ) The Ca 2+ intensity in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( D ) Quantitative analysis of the relative calcium intensity of each group as in C . ( E ) The Ca 2+ signaling in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( F ) Quantitative analysis of the relative calcium intensity of each group as in E . ( G ) Western blotting results of p-MLC and MLC in VSMCs after IAV/H1N1 infection. ( H ) Western blotting results of p-MLC and MLC in VSMCs after IBV/S9-MD infection

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Taurolidine inhibits influenza virus infection and prevents influenza-induced cytokine storm, vasoconstriction and lung damage

doi: 10.1007/s00018-025-05636-6

Figure Lengend Snippet: Taurolidine inhibits intracellular calcium release by influenza virus infection. ( A , B ) The intracellular Ca 2+ concentration was measured after VSMCs cells were infected IAV/H1N1 and IBV/S9-MD, respectively. ( C ) The Ca 2+ intensity in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( D ) Quantitative analysis of the relative calcium intensity of each group as in C . ( E ) The Ca 2+ signaling in IAV/H1N1-infected VSMCs (with or without drug treatment) was measured. ( F ) Quantitative analysis of the relative calcium intensity of each group as in E . ( G ) Western blotting results of p-MLC and MLC in VSMCs after IAV/H1N1 infection. ( H ) Western blotting results of p-MLC and MLC in VSMCs after IBV/S9-MD infection

Article Snippet: The cell suspension and mouse serum were then harvested for Ca 2+ determination performed by a kit from Genmed Scientifics Inc. U.S.A ( GMS50097.1 v.A).

Techniques: Virus, Infection, Concentration Assay, Western Blot

Effect of EGT on intracellular Ca 2+ concentration ([Ca 2+ ] i ) in NE-4C nerve cells. (A) Real-time change of intracellular fluorescence signals with time in NE-4C nerve cells. The stimulation of EGT (1, 10, and 100 μM) started after 30 s of monitoring basal fluorescence intensity. (B) Transient changes of fluorescence from Fluo-4 after stimulation of EGT (1, 10, and 100 μM) in NE-4C nerve cells. Calcium kit II—Fluo 4 was used in this study. Transient changes in [Ca 2+ ] i [relative fluorescence units ,(RFU)] were calculated as the difference between peak ( F max ) and basal ( F 0 ) fluorescence intensity (Δ F = F max – F 0 ) at excitation wavelength of 485 nm, emission wavelength of 525 nm, and cutoff filter of 515 nm. RFU, relative fluorescence units. Values are expressed as the mean ± SD ( n = 3 or 4). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s t -test. * p < 0.05, **** p < 0.0001 vs control.

Journal: ACS Omega

Article Title: Ergothioneine Stimulates Ca 2+ -Mediated Brain-Derived Neurotrophic Factor Expression in NE-4C Nerve Cells

doi: 10.1021/acsomega.4c09920

Figure Lengend Snippet: Effect of EGT on intracellular Ca 2+ concentration ([Ca 2+ ] i ) in NE-4C nerve cells. (A) Real-time change of intracellular fluorescence signals with time in NE-4C nerve cells. The stimulation of EGT (1, 10, and 100 μM) started after 30 s of monitoring basal fluorescence intensity. (B) Transient changes of fluorescence from Fluo-4 after stimulation of EGT (1, 10, and 100 μM) in NE-4C nerve cells. Calcium kit II—Fluo 4 was used in this study. Transient changes in [Ca 2+ ] i [relative fluorescence units ,(RFU)] were calculated as the difference between peak ( F max ) and basal ( F 0 ) fluorescence intensity (Δ F = F max – F 0 ) at excitation wavelength of 485 nm, emission wavelength of 525 nm, and cutoff filter of 515 nm. RFU, relative fluorescence units. Values are expressed as the mean ± SD ( n = 3 or 4). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s t -test. * p < 0.05, **** p < 0.0001 vs control.

Article Snippet: An intracellular Ca 2+ determination kit (Calcium Kit II-Fluo 4; Lot: WQ064) was purchased from DOJINDO Laboratories (Kumamoto, Japan).

Techniques: Concentration Assay, Fluorescence, Control

Structure–activity relationship achieved by contrasting the effect of EGT and its analogues on [Ca 2+ ] i in NE-4C nerve cells. (A) Real-time change of intracellular fluorescence signals with time in NE-4C nerve cells. The stimulation of sample (EGT, ERY, His, and mer-His) started after 30 s of monitoring basal fluorescence intensity. The concentration of each sample is 100 μM. (B) Transient changes of the intracellular fluorescence after sample stimulation in NE-4C nerve cells. Values are expressed as the mean ± SD ( n = 4). Statistical analyses were performed using one-way ANOVA followed by Tukey–Kramer’s t -test among multiple groups. Different letters represent the statistical difference at p < 0.05.

Journal: ACS Omega

Article Title: Ergothioneine Stimulates Ca 2+ -Mediated Brain-Derived Neurotrophic Factor Expression in NE-4C Nerve Cells

doi: 10.1021/acsomega.4c09920

Figure Lengend Snippet: Structure–activity relationship achieved by contrasting the effect of EGT and its analogues on [Ca 2+ ] i in NE-4C nerve cells. (A) Real-time change of intracellular fluorescence signals with time in NE-4C nerve cells. The stimulation of sample (EGT, ERY, His, and mer-His) started after 30 s of monitoring basal fluorescence intensity. The concentration of each sample is 100 μM. (B) Transient changes of the intracellular fluorescence after sample stimulation in NE-4C nerve cells. Values are expressed as the mean ± SD ( n = 4). Statistical analyses were performed using one-way ANOVA followed by Tukey–Kramer’s t -test among multiple groups. Different letters represent the statistical difference at p < 0.05.

Article Snippet: An intracellular Ca 2+ determination kit (Calcium Kit II-Fluo 4; Lot: WQ064) was purchased from DOJINDO Laboratories (Kumamoto, Japan).

Techniques: Activity Assay, Analogues, Fluorescence, Concentration Assay

Involvement of OCTN1 and PHT1 in EGT-or ERY-induced Ca 2+ release in NE-4C nerve cells. (A) Changes in [Ca 2+ ] i in NE-4C nerve cells treated with EGT or ERY (100 μM) in the presence or absence of pyrilamine (antagonist of OCTN1, 0.5 mM). (B) Alternations of [Ca 2+ ] i in NE-4C nerve cells treated with EGT or ERY (100 μM) with or without His (substrate of PHT1, 100 μM). After 30 s of monitoring basal fluorescence intensity, the prepared samples were added to NE-4C nerve cells. Values are expressed as the mean ± SD ( n = 4). Statistical analyses were performed using one-way ANOVA followed by Tukey–Kramer’s t -test among multiple groups. Different letters represent the statistical difference at p < 0.05. OCTN1, organic cation transporter 1; PHT1, peptide/histidine transporter 1.

Journal: ACS Omega

Article Title: Ergothioneine Stimulates Ca 2+ -Mediated Brain-Derived Neurotrophic Factor Expression in NE-4C Nerve Cells

doi: 10.1021/acsomega.4c09920

Figure Lengend Snippet: Involvement of OCTN1 and PHT1 in EGT-or ERY-induced Ca 2+ release in NE-4C nerve cells. (A) Changes in [Ca 2+ ] i in NE-4C nerve cells treated with EGT or ERY (100 μM) in the presence or absence of pyrilamine (antagonist of OCTN1, 0.5 mM). (B) Alternations of [Ca 2+ ] i in NE-4C nerve cells treated with EGT or ERY (100 μM) with or without His (substrate of PHT1, 100 μM). After 30 s of monitoring basal fluorescence intensity, the prepared samples were added to NE-4C nerve cells. Values are expressed as the mean ± SD ( n = 4). Statistical analyses were performed using one-way ANOVA followed by Tukey–Kramer’s t -test among multiple groups. Different letters represent the statistical difference at p < 0.05. OCTN1, organic cation transporter 1; PHT1, peptide/histidine transporter 1.

Article Snippet: An intracellular Ca 2+ determination kit (Calcium Kit II-Fluo 4; Lot: WQ064) was purchased from DOJINDO Laboratories (Kumamoto, Japan).

Techniques: Fluorescence

Effect of intracellular Ca 2+ release channel on EGT-induced increase in [Ca 2+ ] i in NE-4C nerve cells. (A) Effect of 2-APB (inhibitor of IP 3 R) on EGT-stimulated [Ca 2+ ] i changes in NE-4C nerve cells. (B) Impact of 2-APB on ERY-induced [Ca 2+ ] i increase in nerve cells. (C) Effect of dantrolene (inhibitor of RyR) on EGT-stimulated [Ca 2+ ] i upregulation in nerve cells. After 30 s of monitoring basal fluorescence intensity, the prepared samples were added to NE-4C nerve cells. Values are expressed as the mean ± SD ( n = 3 or 4). Statistical analyses were performed using one-way ANOVA followed by Tukey–Kramer’s t -test among multiple groups. Different letters represent the statistical difference at p < 0.05. 2-APB, 2-aminoethoxydiphenyl borate; IP 3 R, inositol 1,4,5-trisphosphate receptor; RyR, ryanodine receptor. 2-APB, 10 μM; EGT, 100 μM; ERY, 100 μM; and dantrolene, 10 μM.

Journal: ACS Omega

Article Title: Ergothioneine Stimulates Ca 2+ -Mediated Brain-Derived Neurotrophic Factor Expression in NE-4C Nerve Cells

doi: 10.1021/acsomega.4c09920

Figure Lengend Snippet: Effect of intracellular Ca 2+ release channel on EGT-induced increase in [Ca 2+ ] i in NE-4C nerve cells. (A) Effect of 2-APB (inhibitor of IP 3 R) on EGT-stimulated [Ca 2+ ] i changes in NE-4C nerve cells. (B) Impact of 2-APB on ERY-induced [Ca 2+ ] i increase in nerve cells. (C) Effect of dantrolene (inhibitor of RyR) on EGT-stimulated [Ca 2+ ] i upregulation in nerve cells. After 30 s of monitoring basal fluorescence intensity, the prepared samples were added to NE-4C nerve cells. Values are expressed as the mean ± SD ( n = 3 or 4). Statistical analyses were performed using one-way ANOVA followed by Tukey–Kramer’s t -test among multiple groups. Different letters represent the statistical difference at p < 0.05. 2-APB, 2-aminoethoxydiphenyl borate; IP 3 R, inositol 1,4,5-trisphosphate receptor; RyR, ryanodine receptor. 2-APB, 10 μM; EGT, 100 μM; ERY, 100 μM; and dantrolene, 10 μM.

Article Snippet: An intracellular Ca 2+ determination kit (Calcium Kit II-Fluo 4; Lot: WQ064) was purchased from DOJINDO Laboratories (Kumamoto, Japan).

Techniques: Fluorescence

Administration of ruthenium red (RR) or Sper protected mice against secondary brain injury and decreased Ca 2+ concentrations after traumatic brain injury (TBI). (A, B, C) Mice were subjected to TBI and then received 1 mg/kg, 3 mg/kg, 5 mg/kg of RR or 2 mg/kg, 5 mg/kg, 10 mg/kg of Sper ip injection or vehicle 30 min after TBI. NSS and Grip test score were evaluated at 1, 3 and 7 days after TBI while brain water content was examined at 1 day after TBI. (A, B) All doses of RR or Sper had an improved motor performance within 3 days; however, larger doses such as 5 mg/kg of RR and 10 mg/kg of Sper did not exhibit a better neuroprotection. This effect was no longer significant at 7 days after TBI, n = 6 per group. (C) Mice subjected to TBI or treated with vehicle had an increased brain water content as compared with the sham group. Brain water content was significantly lower in the groups treated with RR or Sper than the vehicle‐treated group. Moreover, doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect in relieving brain oedema, n = 6 each group. (D) TBI‐induced profound tissue loss of the brain was reversed by RR or Sper, and doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect. (E, F) RR or Sper treatment decreased Ca 2+ concentration following TBI. Restored cellular (E) and mitochondrial (F) concentrations of Ca 2+ by RR (3 mg/kg) or Sper (5 mg/kg) treatment after TBI, n = 6 each group. Data are presented as mean ± SEM; ** P < 0.01, *** P < 0.001 vs sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs TBI + vehicle group. Scale bar: 50 μm

Journal: Journal of Cellular and Molecular Medicine

Article Title: Role of mitochondrial calcium uniporter‐mediated Ca 2+ and iron accumulation in traumatic brain injury

doi: 10.1111/jcmm.14206

Figure Lengend Snippet: Administration of ruthenium red (RR) or Sper protected mice against secondary brain injury and decreased Ca 2+ concentrations after traumatic brain injury (TBI). (A, B, C) Mice were subjected to TBI and then received 1 mg/kg, 3 mg/kg, 5 mg/kg of RR or 2 mg/kg, 5 mg/kg, 10 mg/kg of Sper ip injection or vehicle 30 min after TBI. NSS and Grip test score were evaluated at 1, 3 and 7 days after TBI while brain water content was examined at 1 day after TBI. (A, B) All doses of RR or Sper had an improved motor performance within 3 days; however, larger doses such as 5 mg/kg of RR and 10 mg/kg of Sper did not exhibit a better neuroprotection. This effect was no longer significant at 7 days after TBI, n = 6 per group. (C) Mice subjected to TBI or treated with vehicle had an increased brain water content as compared with the sham group. Brain water content was significantly lower in the groups treated with RR or Sper than the vehicle‐treated group. Moreover, doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect in relieving brain oedema, n = 6 each group. (D) TBI‐induced profound tissue loss of the brain was reversed by RR or Sper, and doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect. (E, F) RR or Sper treatment decreased Ca 2+ concentration following TBI. Restored cellular (E) and mitochondrial (F) concentrations of Ca 2+ by RR (3 mg/kg) or Sper (5 mg/kg) treatment after TBI, n = 6 each group. Data are presented as mean ± SEM; ** P < 0.01, *** P < 0.001 vs sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs TBI + vehicle group. Scale bar: 50 μm

Article Snippet: The mitochondrial and cellular Ca 2+ concentrations were measured by Fura‐3‐AM with a mitochondrial Ca 2+ concentration quantitative determination kit (Genmed Scientifics Inc, USA, catalogue number: GMS10153) and a cellular Ca 2+ concentration quantitative determination kit (Genmed Scientifics Inc, USA, catalogue number: GMS10152).

Techniques: Injection, Concentration Assay

Administration of ruthenium red (RR) or Sper protected mice against secondary brain injury and decreased Ca 2+ concentrations after traumatic brain injury (TBI). (A, B, C) Mice were subjected to TBI and then received 1 mg/kg, 3 mg/kg, 5 mg/kg of RR or 2 mg/kg, 5 mg/kg, 10 mg/kg of Sper ip injection or vehicle 30 min after TBI. NSS and Grip test score were evaluated at 1, 3 and 7 days after TBI while brain water content was examined at 1 day after TBI. (A, B) All doses of RR or Sper had an improved motor performance within 3 days; however, larger doses such as 5 mg/kg of RR and 10 mg/kg of Sper did not exhibit a better neuroprotection. This effect was no longer significant at 7 days after TBI, n = 6 per group. (C) Mice subjected to TBI or treated with vehicle had an increased brain water content as compared with the sham group. Brain water content was significantly lower in the groups treated with RR or Sper than the vehicle‐treated group. Moreover, doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect in relieving brain oedema, n = 6 each group. (D) TBI‐induced profound tissue loss of the brain was reversed by RR or Sper, and doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect. (E, F) RR or Sper treatment decreased Ca 2+ concentration following TBI. Restored cellular (E) and mitochondrial (F) concentrations of Ca 2+ by RR (3 mg/kg) or Sper (5 mg/kg) treatment after TBI, n = 6 each group. Data are presented as mean ± SEM; ** P < 0.01, *** P < 0.001 vs sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs TBI + vehicle group. Scale bar: 50 μm

Journal: Journal of Cellular and Molecular Medicine

Article Title: Role of mitochondrial calcium uniporter‐mediated Ca 2+ and iron accumulation in traumatic brain injury

doi: 10.1111/jcmm.14206

Figure Lengend Snippet: Administration of ruthenium red (RR) or Sper protected mice against secondary brain injury and decreased Ca 2+ concentrations after traumatic brain injury (TBI). (A, B, C) Mice were subjected to TBI and then received 1 mg/kg, 3 mg/kg, 5 mg/kg of RR or 2 mg/kg, 5 mg/kg, 10 mg/kg of Sper ip injection or vehicle 30 min after TBI. NSS and Grip test score were evaluated at 1, 3 and 7 days after TBI while brain water content was examined at 1 day after TBI. (A, B) All doses of RR or Sper had an improved motor performance within 3 days; however, larger doses such as 5 mg/kg of RR and 10 mg/kg of Sper did not exhibit a better neuroprotection. This effect was no longer significant at 7 days after TBI, n = 6 per group. (C) Mice subjected to TBI or treated with vehicle had an increased brain water content as compared with the sham group. Brain water content was significantly lower in the groups treated with RR or Sper than the vehicle‐treated group. Moreover, doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect in relieving brain oedema, n = 6 each group. (D) TBI‐induced profound tissue loss of the brain was reversed by RR or Sper, and doses of 3 mg/kg of RR and 5 mg/kg of Sper had the best effect. (E, F) RR or Sper treatment decreased Ca 2+ concentration following TBI. Restored cellular (E) and mitochondrial (F) concentrations of Ca 2+ by RR (3 mg/kg) or Sper (5 mg/kg) treatment after TBI, n = 6 each group. Data are presented as mean ± SEM; ** P < 0.01, *** P < 0.001 vs sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs TBI + vehicle group. Scale bar: 50 μm

Article Snippet: The mitochondrial and cellular Ca 2+ concentrations were measured by Fura‐3‐AM with a mitochondrial Ca 2+ concentration quantitative determination kit (Genmed Scientifics Inc, USA, catalogue number: GMS10153) and a cellular Ca 2+ concentration quantitative determination kit (Genmed Scientifics Inc, USA, catalogue number: GMS10152).

Techniques: Injection, Concentration Assay

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

Article Title: Tetramethylpyrazine Protects against Early Brain Injury after Experimental Subarachnoid Hemorrhage by Affecting Mitochondrial-Dependent Caspase-3 Apoptotic Pathway

doi: 10.1155/2017/3514914

Figure Lengend Snippet: Ca 2+ concentration in the cytoplasm and mitochondria.

Article Snippet: Next, the Ca 2+ in cytoplasm and mitochondria were, respectively, detected by the Cytoplasmic Ca 2+ Concentration Quantitative Determination Kit (Genmed, USA) and the Mitochondrial Ca 2+ Concentration Quantitative Determination Kit (Genmed, USA).

Techniques: Concentration Assay