Mastitis has severely affected the cattle industry worldwide and has resulted in decreased dairy production and cattle reproduction. Although prevention and treatment methods have been implemented for decades, cattle mastitis is still an intractable disease. Sirtuin 7 (SIRT7) is an NAD+-dependent deacetylase that is involved in various biological processes, including ribosomal RNA synthesis and protein synthesis, DNA damage response, metabolism, and tumorigenesis. However, whether SIRT7 participates in inflammation remains unknown. Our results revealed that SIRT7 is downregulated in tissue samples from mastitic cattle. Therefore, we isolated dairy cow mammary epithelial cells (DCMECs) from breast tissues and developed an in vitro model of lipopolysaccharide- (LPS-) induced inflammation to examine SIRT7 function and its potential role in inflammation. We showed that SIRT7 was significantly downregulated in LPS-treated DCMECs. SIRT7 knockdown significantly increased the LPS-stimulated production of inflammatory mediators, like reactive oxygen and nitric oxide, and upregulated TAB1 and TLR4. In addition, SIRT7 knockdown significantly increased the phosphorylation of TAK1 and NF-κBp65 in LPS-treated DCMECs. Moreover, SIRT7 knockdown promoted the translocation of NF-κBp-p65 to the cell nucleus and then increased the secretion of inflammatory cytokines (IL-1β and IL-6). In contrast, SIRT7 overexpression had the opposite effects when compared to SIRT7 knockdown in LPS-treated DCMECs. In addition, SIRT7 overexpression attenuated LPS-induced DCMEC apoptosis. Taken together, our results indicate that SIRT7 can suppress LPS-induced inflammation and apoptosis via the NF-κB signaling pathway. Therefore, SIRT7 may be considered as a potential pharmacological target for clinical mastitis therapy.
Oxidative stress is involved in the regulation of mammalian reproduction. The present study was conducted to detect the sodium arsenite-induced oxidative stress and alterations in the structure and steroidogenesis in rat ovary. Twenty female adult rats were injected i.p. with sodium arsenite (8 mg/kg BW, T) or 0.9% saline (C) for 16 days. The oxidative stress indexes and morphology of the liver, kidney, and ovary were detected using commercial kits and HE staining, respectively. The serum progesterone and estradiol were detected by RIA, and the ovarian steroidogenic gene expressions were detected by real-time PCR. Results showed that the ovarian activities of SOD and GSH-PX decreased (P < 0.05), while the ROS activity and MDA level increased (P < 0.05) in the T group. HE staining results showed that treatment with sodium arsenite damaged the ovarian morphology, resulting in reduced large and medium follicles and increased atretic follicles. Nonetheless, neither the liver nor kidney showed evident changes in the oxidative stress indexes or morphology after sodium arsenite treatment. The serum progesterone and estradiol levels decreased (P < 0.05) with the reduced expressions in the ovarian steroidogenic genes (StAR, P450scc, and 3β-HSD) (P < 0.05). In conclusion, sodium arsenite injection can induce ovarian oxidative stress in rats which set up an appropriate model for future studies of ovarian diseases as well as the toxic mechanism of arsenic in the reproduction.
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