Dietary alpha-lipoic acid supplementation improves spermatogenesis and semen quality via antioxidant and anti-apoptotic effects in aged breeder roosters
Authors: Ye, Nanwei; Lv, Zengpeng; Dai, Hongjian; Huang, Zhenwu; Shi, Fangxiong
The purpose of the present study was to investigate the effects of dietary alpha-lipoic acid (ALA) supplementation on the reproductive performance of aged breeder roosters. Sixteen 50-wk-old ROSS 308 breeder roosters were randomly allocated to two groups: roosters received a basal diet (CON), or a basal diet supplemented with 300 mg/kg of ALA (ALA). The results indicated that dietary ALA supplementation significantly increased sperm concentration, motility, viability, and membrane functional integrity. ALA also dramatically increased seminiferous tubule epithelial height (SEH) and testis scores. The ALA group had a higher serum concentration of testosterone than the CON group. ALA supplementation remarkably increased total antioxidant capacity (T-AOC), the enzyme activities of glutathione peroxidase (GPx), and catalase (CAT) in the testes; following a decrease in malondialdehyde (MDA) levels. In addition, we noted significant upregulation of Nrf2 mRNA and protein expression of and mRNA expression of its Downstream Genes (GPx1, NQO1, and GCLC), as well as significant downregulation of Keap1 mRNA expression in testicular tissue of aged roosters with ALA supplementation. The protein expression of Caspase 3 was downregulated and the protein expression of proliferating cell nuclear antigen (PCNA) was upregulated by ALA supplementation. The mRNA expression of spermatogenesis-related genes (ER1, AKT1, and Cav1) were markedly augmented in the ALA group compared with the CON group. In conclusion, dietary ALA supplementation enhanced the testicular antioxidant capacity through the Nrf2-signaling pathway, exerted anti-apoptotic effects, and improved the reproductive performance of aged roosters. (C) 2020 Elsevier Inc. All rights reserved.
Shenmai Injection Upregulates Heme Oxygenase-1 to Confer Protection Against Severe Acute Pancreatitis
JOURNAL OF SURGICAL RESEARCH
Authors: Zhang, Fei-hu; Liu, Yang; Dong, Xiao-bin; Hao, Hao; Fan, Kai-liang; Meng, Xian-qing; Kong, Li
Background: To explore the mechanism of Shenmai injection (SMI) on severe acute pancreatitis (SAP) through heme oxygenase-1 (HO-1) signaling. Methods: A total of 40 male Sprague-Dawley (SD) rats (220-260 g) were grouped into the following four categories (n = 10): SAP + SMI + Zinc protoporphyrin (ZnPP), SAP + SMI, SAP, and sham surgery groups. ZnPP is a specific inhibitor of HO-1. Four percent of sodium taurocholate (1 mL/kg) was retrogradely injected via the pancreatic duct to induce the SAP model. The SAP group rats received 1.6 mL/kg saline by intravenous injection 30 min after the induction of SAP. The SAP + SMI group rats received 1.6 mL/kg SMI by intravenous injection 30 min after the induction of SAP. The SAP + SMI + ZnPP group rats received an intravenous injection of 1.6 mL/kg SMI and intraperitoneal administration of 30 mg/kg ZnPP 30 min after the SAP induction. Twenty-four hours after the SAP induction, blood samples were collected for the measurement of amylase, lipase, creatinine, myeloperoxidase, interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-alpha), and HO-1 level, while tissue specimens were harvested for the determination of HO-1, TNF-alpha, and IL-10 mRNA level. Meanwhile, histopathological changes in organs (pancreas, lung, and kidney) were stored. Results: The serum concentration of amylase, lipase, creatinine, and myeloperoxidase was higher in the SAP group than in the SAP + SMI group. Treatment with SMI increased HO-1 and IL-10 level and reduced TNF-alpha level in serumand tissues compared to the SAP group (P<0.05). Treatment with SMI abolished the organ-damaging effects of SAP (P < 0.05). Furthermore, suppression of HO-1 expression by ZnPP canceled the aforementioned effects. Conclusions: SMI confers protection against the SAP-induced systemic inflammatory response and multiple organs damage via HO-1 upregulation. (C) 2020 The Authors. Published by Elsevier Inc.