Hydrogen sulfide repairs testicular damage induced by heat stress in rats
Heat stress can cause testicular damage and affect male fertility. The gasotransmitter hydrogen sulfide (H2S) is involved in various physiological and pathophysiological processes, with antioxidant and anti‐inflammation effects. The aim of this study was to investigate whether H2S could reduce the t...
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| Format: | Article |
| Language: | English |
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Wiley
2025-06-01
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| Series: | FEBS Open Bio |
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| Online Access: | https://doi.org/10.1002/2211-5463.70010 |
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| author | Xinyu Guo Yupeng Yin Susu Guo Xiaoyan Chen Suyan Xie Shiqin Chen Yan Huang |
| author_facet | Xinyu Guo Yupeng Yin Susu Guo Xiaoyan Chen Suyan Xie Shiqin Chen Yan Huang |
| author_sort | Xinyu Guo |
| collection | DOAJ |
| description | Heat stress can cause testicular damage and affect male fertility. The gasotransmitter hydrogen sulfide (H2S) is involved in various physiological and pathophysiological processes, with antioxidant and anti‐inflammation effects. The aim of this study was to investigate whether H2S could reduce the testicular damage caused by heat stress. In this study, we constructed a rat heat‐stress model and treated it with H2S. Histopathology, high‐throughput sequencing, bioinformatics analysis and molecular biology methods were used to investigate whether H2S donor NaHS could alleviate heat stress‐induced testicular injury and to explore the underlying mode of action of H2S. Heat stress reduced testis index, sperm quality, sex hormone levels and disturbed testicular structures. High‐throughput transcriptome sequencing and Gene Ontology (GO) enrichment analyses showed that genes involved in inflammation were upregulated in the heat stress group compared to the control group. H2S treatment increased testis index, sperm quality and attenuated pathological alternation and hormone disorder in rats exposed to heat stress. Furthermore, H2S administration reversed increased inflammatory factors tumor necrosis factor‐α, interleukin‐1β and interleukin‐6, and resulted in a significant decrease in malondialdehyde levels and in increased activity of catalase and ratio of reduced/oxidized glutathione compared to the heat stress group. This study suggests that H2S donor NaHS can effectively restore testicular damage caused by heat stress in rats by inhibiting inflammation and oxidative stress. |
| format | Article |
| id | doaj-art-c0334013d47146d5a572991deef8653c |
| institution | OA Journals |
| issn | 2211-5463 |
| language | English |
| publishDate | 2025-06-01 |
| publisher | Wiley |
| record_format | Article |
| series | FEBS Open Bio |
| spelling | doaj-art-c0334013d47146d5a572991deef8653c2025-08-20T02:23:53ZengWileyFEBS Open Bio2211-54632025-06-0115696397110.1002/2211-5463.70010Hydrogen sulfide repairs testicular damage induced by heat stress in ratsXinyu Guo0Yupeng Yin1Susu Guo2Xiaoyan Chen3Suyan Xie4Shiqin Chen5Yan Huang6Center of Reproductive Medicine The General Hospital of Southern Theater Command Guangzhou ChinaDepartment of Obstetrics and Gynecology General Hospital of Southern Theatre Command Guangzhou ChinaCenter of Reproductive Medicine The General Hospital of Southern Theater Command Guangzhou ChinaCenter of Reproductive Medicine The General Hospital of Southern Theater Command Guangzhou ChinaCenter of Reproductive Medicine The General Hospital of Southern Theater Command Guangzhou ChinaCenter of Reproductive Medicine The General Hospital of Southern Theater Command Guangzhou ChinaCenter of Reproductive Medicine The General Hospital of Southern Theater Command Guangzhou ChinaHeat stress can cause testicular damage and affect male fertility. The gasotransmitter hydrogen sulfide (H2S) is involved in various physiological and pathophysiological processes, with antioxidant and anti‐inflammation effects. The aim of this study was to investigate whether H2S could reduce the testicular damage caused by heat stress. In this study, we constructed a rat heat‐stress model and treated it with H2S. Histopathology, high‐throughput sequencing, bioinformatics analysis and molecular biology methods were used to investigate whether H2S donor NaHS could alleviate heat stress‐induced testicular injury and to explore the underlying mode of action of H2S. Heat stress reduced testis index, sperm quality, sex hormone levels and disturbed testicular structures. High‐throughput transcriptome sequencing and Gene Ontology (GO) enrichment analyses showed that genes involved in inflammation were upregulated in the heat stress group compared to the control group. H2S treatment increased testis index, sperm quality and attenuated pathological alternation and hormone disorder in rats exposed to heat stress. Furthermore, H2S administration reversed increased inflammatory factors tumor necrosis factor‐α, interleukin‐1β and interleukin‐6, and resulted in a significant decrease in malondialdehyde levels and in increased activity of catalase and ratio of reduced/oxidized glutathione compared to the heat stress group. This study suggests that H2S donor NaHS can effectively restore testicular damage caused by heat stress in rats by inhibiting inflammation and oxidative stress.https://doi.org/10.1002/2211-5463.70010H2Sheat stressinflammationoxidative stresstestis |
| spellingShingle | Xinyu Guo Yupeng Yin Susu Guo Xiaoyan Chen Suyan Xie Shiqin Chen Yan Huang Hydrogen sulfide repairs testicular damage induced by heat stress in rats FEBS Open Bio H2S heat stress inflammation oxidative stress testis |
| title | Hydrogen sulfide repairs testicular damage induced by heat stress in rats |
| title_full | Hydrogen sulfide repairs testicular damage induced by heat stress in rats |
| title_fullStr | Hydrogen sulfide repairs testicular damage induced by heat stress in rats |
| title_full_unstemmed | Hydrogen sulfide repairs testicular damage induced by heat stress in rats |
| title_short | Hydrogen sulfide repairs testicular damage induced by heat stress in rats |
| title_sort | hydrogen sulfide repairs testicular damage induced by heat stress in rats |
| topic | H2S heat stress inflammation oxidative stress testis |
| url | https://doi.org/10.1002/2211-5463.70010 |
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