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3β-HSD and P450 expression in BTV-1 experimentally infected rams and mock-infected controls. (A and B) Immunohistochemistry showing expression of 3β-HSD (A) and P450 (B) (in brown) by the Leydig cells in sections of the testes of mock-infected healthy control rams. Arrows point to Leydig cells. (C to F) Immunohistochemistry showing lack of expression of 3β-HSD (C and E) and P450 (D and F) by Leydig cells in the testes of rams infected with BTV-1 IT2006 (C and D) or BTV-1 IT2013 (E and F). The peritubular areas where the Leydig cells are located are highlighted with a broken line. Scale bars, 100 μm. (G) Graph representing the relative levels of <t>testosterone,</t> assessed by <t>ELISA,</t> in the blood of rams infected with either BTV-1 IT2006 or BTV-1 IT2013 . Values are shown as percentages of the values of testosterone taken at day 0 before virus infection. Note the significant reduction in the levels of testosterone in rams infected with BTV-1 IT2006 between 0 and 8 to 11 dpi ( P < 0.05; one-way ANOVA) and in rams infected with BTV-1 IT2013 between 0 and either 5 or 15 dpi ( P < 0.05; one-way ANOVA).
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of <t>testosterone</t> in serum was detected by <t>ELISA</t> kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.
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Data of intraprostatic hormone concentrations and apoptosis induced by PAO compared with control at 6-month of follow-up
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Data of intraprostatic hormone concentrations and apoptosis induced by PAO compared with control at 6-month of follow-up
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Image Search Results


3β-HSD and P450 expression in BTV-1 experimentally infected rams and mock-infected controls. (A and B) Immunohistochemistry showing expression of 3β-HSD (A) and P450 (B) (in brown) by the Leydig cells in sections of the testes of mock-infected healthy control rams. Arrows point to Leydig cells. (C to F) Immunohistochemistry showing lack of expression of 3β-HSD (C and E) and P450 (D and F) by Leydig cells in the testes of rams infected with BTV-1 IT2006 (C and D) or BTV-1 IT2013 (E and F). The peritubular areas where the Leydig cells are located are highlighted with a broken line. Scale bars, 100 μm. (G) Graph representing the relative levels of testosterone, assessed by ELISA, in the blood of rams infected with either BTV-1 IT2006 or BTV-1 IT2013 . Values are shown as percentages of the values of testosterone taken at day 0 before virus infection. Note the significant reduction in the levels of testosterone in rams infected with BTV-1 IT2006 between 0 and 8 to 11 dpi ( P < 0.05; one-way ANOVA) and in rams infected with BTV-1 IT2013 between 0 and either 5 or 15 dpi ( P < 0.05; one-way ANOVA).

Journal: Journal of Virology

Article Title: Testicular Degeneration and Infertility following Arbovirus Infection

doi: 10.1128/JVI.01131-18

Figure Lengend Snippet: 3β-HSD and P450 expression in BTV-1 experimentally infected rams and mock-infected controls. (A and B) Immunohistochemistry showing expression of 3β-HSD (A) and P450 (B) (in brown) by the Leydig cells in sections of the testes of mock-infected healthy control rams. Arrows point to Leydig cells. (C to F) Immunohistochemistry showing lack of expression of 3β-HSD (C and E) and P450 (D and F) by Leydig cells in the testes of rams infected with BTV-1 IT2006 (C and D) or BTV-1 IT2013 (E and F). The peritubular areas where the Leydig cells are located are highlighted with a broken line. Scale bars, 100 μm. (G) Graph representing the relative levels of testosterone, assessed by ELISA, in the blood of rams infected with either BTV-1 IT2006 or BTV-1 IT2013 . Values are shown as percentages of the values of testosterone taken at day 0 before virus infection. Note the significant reduction in the levels of testosterone in rams infected with BTV-1 IT2006 between 0 and 8 to 11 dpi ( P < 0.05; one-way ANOVA) and in rams infected with BTV-1 IT2013 between 0 and either 5 or 15 dpi ( P < 0.05; one-way ANOVA).

Article Snippet: The concentration of testosterone in the sera of BTV-1 IT2006 - and BTV-1 IT2013 -infected rams was measured using a sheep testosterone ELISA kit (Shanghai Korain Biothec Co., China) according to the manufacturer's instructions.

Techniques: Expressing, Infection, Immunohistochemistry, Control, Enzyme-linked Immunosorbent Assay, Virus

Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of testosterone in serum was detected by ELISA kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.

Journal: Ecotoxicology and environmental safety

Article Title: Ameliorative effect of betulinic acid against zearalenone exposure triggers testicular dysfunction and oxidative stress in mice via p38/ERK MAPK inhibition and Nrf2-mediated antioxidant defense activation.

doi: 10.1016/j.ecoenv.2022.113561

Figure Lengend Snippet: Fig. 2. BA protected the aggravation of male reproduction injury in ZEA-induced mice. The morphology of the sperm was photographed using an optical microscope (A). The sperm motility was used to evaluate the male repro duction of mice, including sperm survival rate (B), sperm malformation rate (C), and sperm mortality rate (D). Protein and mRNA levels of ERα in testis were detected by immunoblotting and RT-PCR analysis, respectively, and the pro tein and mRNA levels were normalized to β-actin (E-G). The content of testosterone in serum was detected by ELISA kit (H). The mRNA expression of CLDN11 (I), CDH2 (J), and Vim (K) were measured by RT-PCR. Mean ± SEM, *P < 0.05 and **P < 0.01 represented a significant differ ence compared to the control group, while #P < 0.05 and ##P < 0.01 represented a signifi cant difference compared to the ZEA group.

Article Snippet: Testosterone enzyme linked immunosorbent assay (ELISA) kit (CSB-E05101m) was obtained from Cusabio Biotech Co. Ltd. (Wuhan, China).

Techniques: Microscopy, Western Blot, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Expressing, Control

Data of intraprostatic hormone concentrations and apoptosis induced by PAO compared with control at 6-month of follow-up

Journal: Translational Andrology and Urology

Article Title: Prostatic artery occlusion: initial findings on pathophysiological response in a canine prostate model

doi: 10.21037/tau-22-423

Figure Lengend Snippet: Data of intraprostatic hormone concentrations and apoptosis induced by PAO compared with control at 6-month of follow-up

Article Snippet: Canine testosterone was measured using a solid phase sandwich ELISA method [Canine Testosterone (T) ELISAN Kit, CUSABIO, Wuhan Hi-tech Medical Devices Park, Wuhan, Hubei Province, China].

Techniques: Control, TUNEL Assay