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( a ) A part of the testicular biopsy obtained from a man with OA. <t>Testosterone</t> expression (→) in Leydig cells showed a fine granular pattern (Bv, blood vessel) (DAB, ×400, scale = 25 µm); ( b ) Testosterone expression (→) in a testicular biopsy from a patient with Sertoli cells only syndrome. Solely Leydig cells were positive. Seminiferous tubule was lacking spermatogenic cells. (DAB, ×400, scale = 25 µm).
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( a ) A part of the testicular biopsy obtained from a man with OA. <t>Testosterone</t> expression (→) in Leydig cells showed a fine granular pattern (Bv, blood vessel) (DAB, ×400, scale = 25 µm); ( b ) Testosterone expression (→) in a testicular biopsy from a patient with Sertoli cells only syndrome. Solely Leydig cells were positive. Seminiferous tubule was lacking spermatogenic cells. (DAB, ×400, scale = 25 µm).
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Figure 1. Morphology and Histopathology of the Genital Tracts in Male Mice Infected with ZIKV (A) Morphology of the male genital tract from an uninfected WT mouse. T (testis), SV (seminal vesicle), VP (ventral prostate), VD (vas deferens), EP (epididymis). (B) Morphology of the male genital tract from an uninfected KO mouse. (C) Morphology of the male genital tract from a KO mouse IP infected with ZIKV at 8 DPI (n = 10). Scale bar, 0.5 cm in A, B, and C. The mice from A–C are age matched. (D1) Testis. (E1) Caput epididymis. (F1) Corpus epididymis. (G1) Cauda epididymis. (H1) Ventral prostate. (I1) Seminal vesicle. D1–H1 are representative images from a WT male mouse given PBS by IP (n = 10). (D2) Testis. (E2) Caput epididymis. (F2) Corpus epididymis and (G2) Cauda epididymis. (H2) Ventral prostate and (I2) Seminal vesicle. D2–H2 are representative images from a KO mouse given PBS (n = 10). (D3) Testis. (E3) Caput epididymis. (F3) Corpus epididymis and (G3) Cauda epididymis. (H3) Ventral prostate. (I3) Seminal vesicle. D3–I3 from a WT mouse IP infected with ZIKV (n = 10) at 8 DPI. Abnormalities were not observed. (J) Histological analysis of the testes from ZIKV-infected KO mice. (K) Higher magni- fication of the testis inside the rectangle from D1 (403). Normal seminiferous tubules with different steps of germinal epithelial cells (bigger black arrows) in order and normal intratesticular capillary (white arrow) neighbored with normal <t>testosterone-producing</t> LC (smaller black arrow) in WT testis. (L) Higher magnification of the testis inside the rectangle from D2 (403). Normal seminiferous tubules with different steps of germinal epithelial cells and normal intratesticular capillary (white arrow), neighbored with normal testosterone-producing LC (smaller black arrow) in KO testis. (M) Disrupted seminiferous tubules with cells out of order, different degenerating germinal epithelial cells (bigger black arrows) inside the seminiferous tubules of the ZIKV-infected testes, intratesticular varicoceles/congestion (white arrow), lymphocyte infiltrations (smaller arrows), and necrotic LC (black arrowheads) surrounded by lymphocytes were observed within the interstitium from ZIKV-infected KO testes. (N–P) (N) Caput epididymis. (O) Corpus epididymis and (P) Cauda epididymis. (N–P) Epididymis from ZIKV-infected KO mice. The
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Figure 1. Morphology and Histopathology of the Genital Tracts in Male Mice Infected with ZIKV (A) Morphology of the male genital tract from an uninfected WT mouse. T (testis), SV (seminal vesicle), VP (ventral prostate), VD (vas deferens), EP (epididymis). (B) Morphology of the male genital tract from an uninfected KO mouse. (C) Morphology of the male genital tract from a KO mouse IP infected with ZIKV at 8 DPI (n = 10). Scale bar, 0.5 cm in A, B, and C. The mice from A–C are age matched. (D1) Testis. (E1) Caput epididymis. (F1) Corpus epididymis. (G1) Cauda epididymis. (H1) Ventral prostate. (I1) Seminal vesicle. D1–H1 are representative images from a WT male mouse given PBS by IP (n = 10). (D2) Testis. (E2) Caput epididymis. (F2) Corpus epididymis and (G2) Cauda epididymis. (H2) Ventral prostate and (I2) Seminal vesicle. D2–H2 are representative images from a KO mouse given PBS (n = 10). (D3) Testis. (E3) Caput epididymis. (F3) Corpus epididymis and (G3) Cauda epididymis. (H3) Ventral prostate. (I3) Seminal vesicle. D3–I3 from a WT mouse IP infected with ZIKV (n = 10) at 8 DPI. Abnormalities were not observed. (J) Histological analysis of the testes from ZIKV-infected KO mice. (K) Higher magni- fication of the testis inside the rectangle from D1 (403). Normal seminiferous tubules with different steps of germinal epithelial cells (bigger black arrows) in order and normal intratesticular capillary (white arrow) neighbored with normal <t>testosterone-producing</t> LC (smaller black arrow) in WT testis. (L) Higher magnification of the testis inside the rectangle from D2 (403). Normal seminiferous tubules with different steps of germinal epithelial cells and normal intratesticular capillary (white arrow), neighbored with normal testosterone-producing LC (smaller black arrow) in KO testis. (M) Disrupted seminiferous tubules with cells out of order, different degenerating germinal epithelial cells (bigger black arrows) inside the seminiferous tubules of the ZIKV-infected testes, intratesticular varicoceles/congestion (white arrow), lymphocyte infiltrations (smaller arrows), and necrotic LC (black arrowheads) surrounded by lymphocytes were observed within the interstitium from ZIKV-infected KO testes. (N–P) (N) Caput epididymis. (O) Corpus epididymis and (P) Cauda epididymis. (N–P) Epididymis from ZIKV-infected KO mice. The
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Figure 1. Morphology and Histopathology of the Genital Tracts in Male Mice Infected with ZIKV (A) Morphology of the male genital tract from an uninfected WT mouse. T (testis), SV (seminal vesicle), VP (ventral prostate), VD (vas deferens), EP (epididymis). (B) Morphology of the male genital tract from an uninfected KO mouse. (C) Morphology of the male genital tract from a KO mouse IP infected with ZIKV at 8 DPI (n = 10). Scale bar, 0.5 cm in A, B, and C. The mice from A–C are age matched. (D1) Testis. (E1) Caput epididymis. (F1) Corpus epididymis. (G1) Cauda epididymis. (H1) Ventral prostate. (I1) Seminal vesicle. D1–H1 are representative images from a WT male mouse given PBS by IP (n = 10). (D2) Testis. (E2) Caput epididymis. (F2) Corpus epididymis and (G2) Cauda epididymis. (H2) Ventral prostate and (I2) Seminal vesicle. D2–H2 are representative images from a KO mouse given PBS (n = 10). (D3) Testis. (E3) Caput epididymis. (F3) Corpus epididymis and (G3) Cauda epididymis. (H3) Ventral prostate. (I3) Seminal vesicle. D3–I3 from a WT mouse IP infected with ZIKV (n = 10) at 8 DPI. Abnormalities were not observed. (J) Histological analysis of the testes from ZIKV-infected KO mice. (K) Higher magni- fication of the testis inside the rectangle from D1 (403). Normal seminiferous tubules with different steps of germinal epithelial cells (bigger black arrows) in order and normal intratesticular capillary (white arrow) neighbored with normal <t>testosterone-producing</t> LC (smaller black arrow) in WT testis. (L) Higher magnification of the testis inside the rectangle from D2 (403). Normal seminiferous tubules with different steps of germinal epithelial cells and normal intratesticular capillary (white arrow), neighbored with normal testosterone-producing LC (smaller black arrow) in KO testis. (M) Disrupted seminiferous tubules with cells out of order, different degenerating germinal epithelial cells (bigger black arrows) inside the seminiferous tubules of the ZIKV-infected testes, intratesticular varicoceles/congestion (white arrow), lymphocyte infiltrations (smaller arrows), and necrotic LC (black arrowheads) surrounded by lymphocytes were observed within the interstitium from ZIKV-infected KO testes. (N–P) (N) Caput epididymis. (O) Corpus epididymis and (P) Cauda epididymis. (N–P) Epididymis from ZIKV-infected KO mice. The
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Cusabio testosterone enzyme linked immunosorbent assay elisa kit
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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Image Search Results


( a ) A part of the testicular biopsy obtained from a man with OA. Testosterone expression (→) in Leydig cells showed a fine granular pattern (Bv, blood vessel) (DAB, ×400, scale = 25 µm); ( b ) Testosterone expression (→) in a testicular biopsy from a patient with Sertoli cells only syndrome. Solely Leydig cells were positive. Seminiferous tubule was lacking spermatogenic cells. (DAB, ×400, scale = 25 µm).

Journal: Life

Article Title: Leydig Cells in Patients with Non-Obstructive Azoospermia: Do They Really Proliferate?

doi: 10.3390/life11111266

Figure Lengend Snippet: ( a ) A part of the testicular biopsy obtained from a man with OA. Testosterone expression (→) in Leydig cells showed a fine granular pattern (Bv, blood vessel) (DAB, ×400, scale = 25 µm); ( b ) Testosterone expression (→) in a testicular biopsy from a patient with Sertoli cells only syndrome. Solely Leydig cells were positive. Seminiferous tubule was lacking spermatogenic cells. (DAB, ×400, scale = 25 µm).

Article Snippet: The presence of Leydig cells was confirmed with two antibodies: against the antigen INSL3 (HPA028615, Sigma Aldrich, Taufkirchen, Germany, dilution 1:100) and testosterone (NBP2-45187, Novus Biologicals, Littleton, CO, USA, dilution 1:20).

Techniques: Expressing

Figure 1. Morphology and Histopathology of the Genital Tracts in Male Mice Infected with ZIKV (A) Morphology of the male genital tract from an uninfected WT mouse. T (testis), SV (seminal vesicle), VP (ventral prostate), VD (vas deferens), EP (epididymis). (B) Morphology of the male genital tract from an uninfected KO mouse. (C) Morphology of the male genital tract from a KO mouse IP infected with ZIKV at 8 DPI (n = 10). Scale bar, 0.5 cm in A, B, and C. The mice from A–C are age matched. (D1) Testis. (E1) Caput epididymis. (F1) Corpus epididymis. (G1) Cauda epididymis. (H1) Ventral prostate. (I1) Seminal vesicle. D1–H1 are representative images from a WT male mouse given PBS by IP (n = 10). (D2) Testis. (E2) Caput epididymis. (F2) Corpus epididymis and (G2) Cauda epididymis. (H2) Ventral prostate and (I2) Seminal vesicle. D2–H2 are representative images from a KO mouse given PBS (n = 10). (D3) Testis. (E3) Caput epididymis. (F3) Corpus epididymis and (G3) Cauda epididymis. (H3) Ventral prostate. (I3) Seminal vesicle. D3–I3 from a WT mouse IP infected with ZIKV (n = 10) at 8 DPI. Abnormalities were not observed. (J) Histological analysis of the testes from ZIKV-infected KO mice. (K) Higher magni- fication of the testis inside the rectangle from D1 (403). Normal seminiferous tubules with different steps of germinal epithelial cells (bigger black arrows) in order and normal intratesticular capillary (white arrow) neighbored with normal testosterone-producing LC (smaller black arrow) in WT testis. (L) Higher magnification of the testis inside the rectangle from D2 (403). Normal seminiferous tubules with different steps of germinal epithelial cells and normal intratesticular capillary (white arrow), neighbored with normal testosterone-producing LC (smaller black arrow) in KO testis. (M) Disrupted seminiferous tubules with cells out of order, different degenerating germinal epithelial cells (bigger black arrows) inside the seminiferous tubules of the ZIKV-infected testes, intratesticular varicoceles/congestion (white arrow), lymphocyte infiltrations (smaller arrows), and necrotic LC (black arrowheads) surrounded by lymphocytes were observed within the interstitium from ZIKV-infected KO testes. (N–P) (N) Caput epididymis. (O) Corpus epididymis and (P) Cauda epididymis. (N–P) Epididymis from ZIKV-infected KO mice. The

Journal: Cell

Article Title: Zika Virus Causes Testis Damage and Leads to Male Infertility in Mice.

doi: 10.1016/j.cell.2016.11.016

Figure Lengend Snippet: Figure 1. Morphology and Histopathology of the Genital Tracts in Male Mice Infected with ZIKV (A) Morphology of the male genital tract from an uninfected WT mouse. T (testis), SV (seminal vesicle), VP (ventral prostate), VD (vas deferens), EP (epididymis). (B) Morphology of the male genital tract from an uninfected KO mouse. (C) Morphology of the male genital tract from a KO mouse IP infected with ZIKV at 8 DPI (n = 10). Scale bar, 0.5 cm in A, B, and C. The mice from A–C are age matched. (D1) Testis. (E1) Caput epididymis. (F1) Corpus epididymis. (G1) Cauda epididymis. (H1) Ventral prostate. (I1) Seminal vesicle. D1–H1 are representative images from a WT male mouse given PBS by IP (n = 10). (D2) Testis. (E2) Caput epididymis. (F2) Corpus epididymis and (G2) Cauda epididymis. (H2) Ventral prostate and (I2) Seminal vesicle. D2–H2 are representative images from a KO mouse given PBS (n = 10). (D3) Testis. (E3) Caput epididymis. (F3) Corpus epididymis and (G3) Cauda epididymis. (H3) Ventral prostate. (I3) Seminal vesicle. D3–I3 from a WT mouse IP infected with ZIKV (n = 10) at 8 DPI. Abnormalities were not observed. (J) Histological analysis of the testes from ZIKV-infected KO mice. (K) Higher magni- fication of the testis inside the rectangle from D1 (403). Normal seminiferous tubules with different steps of germinal epithelial cells (bigger black arrows) in order and normal intratesticular capillary (white arrow) neighbored with normal testosterone-producing LC (smaller black arrow) in WT testis. (L) Higher magnification of the testis inside the rectangle from D2 (403). Normal seminiferous tubules with different steps of germinal epithelial cells and normal intratesticular capillary (white arrow), neighbored with normal testosterone-producing LC (smaller black arrow) in KO testis. (M) Disrupted seminiferous tubules with cells out of order, different degenerating germinal epithelial cells (bigger black arrows) inside the seminiferous tubules of the ZIKV-infected testes, intratesticular varicoceles/congestion (white arrow), lymphocyte infiltrations (smaller arrows), and necrotic LC (black arrowheads) surrounded by lymphocytes were observed within the interstitium from ZIKV-infected KO testes. (N–P) (N) Caput epididymis. (O) Corpus epididymis and (P) Cauda epididymis. (N–P) Epididymis from ZIKV-infected KO mice. The

Article Snippet: The ELISA kits for IFNb (42400) and for mouse testosterone (DEV 9911) were purchased from R&D Systems (R&D Systems, US) and Demedtec (Kiel-Wellsee, Germany), respectively.

Techniques: Histopathology, Infection

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