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Immunolocalization of IL-6 and IL-10 in the testicular tissue of testicular dysfunction rat treated with secretome

ABSTRACT: Objective: This study was carried out to find out the immunolocalization of Interleukin 6 (IL-6) and Interleukin 10 (IL-10) in the testicular tissue of testicular dysfunction rat treated with secretome from human umbilical stem cells. Materials and methods: Rats were induced with cisplatin for testicular dysfunction condition. After that, the rats were grouped into two categories and were treated with secretome at 0.2 and 0.5 ml/kg BW once every week for 4 weeks. One week later, after the secretome treatment, the rats were sacrificed for histological evaluation using the immunohistochemical method. The preparation slides were examined using a light microscope and were analyzed descriptively and quantitatively. Results: There were no IL-6 and IL-10 immunoreactivities seen in the testicular tissue after cisplatin induction. However, the immunoreactivities of IL-6 and IL-10 were detected after secretome treatment, with both dosages of 0.2 and 0.5 ml/kg BW. These immunoreactivities were detected in the spermatogonia, spermatid/luminal tissue of seminiferous tubule, spermatogenic cells, and Leydig cells. In the cell calculation, the numbers of IL-6 immunoreactive cells were higher at the lower secretome dosage. In contrast, the numbers of IL-10 immunoreactive cells were higher at the higher secretome dosage. Conclusion: IL-6 and IL-10 can be localized in the testicular tissue of testicular dysfunction rat after secretome treatment.

SUBMITTER: Prihatno S

PROVIDER: S-EPMC7521813 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Project description:Functional phenotypes, which cells can acquire depending on the microenvironment, are currently the focus of investigations into new anti-inflammatory therapeutic approaches. Glial cells, microglia, and astrocytes are major participants in neuroinflammation, but their roles differ, as microglia are cells of mesodermal origin, while astrocytes are cells of ectodermal origin. The inflammatory phenotype of cells can be modulated by ?-6- and ?-3-polyunsaturated fatty acid-derived oxylipins, although data on changes in oxylipin profiles in different cell adaptations to pro- and anti-inflammatory stimuli are scarce. Our study aimed to compare UPLC-MS/MS-measured oxylipin profiles in various rat astrocyte adaptation states. We used cells treated for 24 h with lipopolysaccharide (LPS) for classical pro-inflammatory adaptation and with interleukin 4 (IL-4) or 10 (IL-10) for alternative anti-inflammatory adaptation, with the resulting phenotypes characterized by quantitative real-time PCR (RT-PCR). We also tested long-term, low-concentration LPS treatment (endotoxin treatment) as a model of astrocyte adaptations. The functional response of astrocytes was estimated by acute (4 h) LPS-induced cell reactivity, measured by gene expression markers and oxylipin synthesis. We discovered that, as well as gene markers, oxylipin profiles can serve as markers of pro- (A1-like) or anti-inflammatory (A2-like) adaptations. We observed predominant involvement of ?-6 polyunsaturated fatty acid (PUFA) and the cyclooxygenase branch for classical (LPS) pro-inflammatory adaptations and ?-3 PUFA and the lipoxygenase branch for alternative (IL-4) anti-inflammatory adaptations. Treatment with IL-4, but not IL-10, primes the ability of astrocytes to activate the innate immunity signaling pathways in response to LPS. Endotoxin-treated astrocytes provide an alternative anti-inflammatory adaptation, which makes cells less sensitive to acute LPS stimulation than the IL-4 induced adaptation. Taken together, the data reveal that oxylipin profiles associate with different states of polarization to generate a pro-inflammatory or anti-inflammatory phenotype. This association manifests itself both in native cells and in their responses to a pro-inflammatory stimulus.

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Immunolocalization of IL-6 and IL-10 in the testicular tissue of testicular dysfunction rat treated with secretome

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