Deeper insight into maternal genetic assessments and demographic history for Egyptian indigenous chicken populations using mtDNA analysis

This study principally sought to reveal the demographic expansion of Egyptian indigenous chickens (EIC) using representative breeds: Sinai (North), Fayoumi (Middle) and Dandarawi (South) of Egypt as well as to deeply clarify their genetic diversity, possible matrilineal origin and dispersal routes. A total of 33 partial mitochondrial DNA sequences were generated from EIC and compared with a worldwide reference dataset of 1290 wild and domestic chicken sequences. Study populations had 12 polymorphic variable sites and 7 haplotypes. A lack of maternal substructure between EIC was detected (FST = 0.003). The unimodal mismatch distribution and negative values of Tajima’s D (−0.659) and Fu’s Fs (−0.157) indicated demographic expansion among EIC and pointed to Fayoumi as the oldest EIC population. Egyptian haplotypes were clustered phylogenetically into two divergent clades. Their phylogeography revealed an ancient single maternal lineage of Egyptian chickens likely derived from Indian-Subcontinent. Moreover, a recent maternal commercial heritage possibly originated in Yunnan-Province and/or surrounding areas was admixed restrictedly into Sinai. It is implied that Egypt was an entry point for Indian chicken into Africa and its further dispersal route to Europe. This study provides a clue supporting the previous assumption that urged utilizing consistent founder populations having closely related progenitors for synthetizing a stabilized homogenous crossbreed as a sustainable discipline in breeding program

Ameliorating effect of probiotic on nonalcoholic fatty liver disease and lipolytic gene expression in rabbits

Abstract Nonalcoholic fatty liver disease (NAFLD) is a condition that affects about 24% of people worldwide. Increased liver fat, inflammation, and, in the most severe cases, cell death are all characteristics of NAFLD. However, NAFLD pathogenesis and therapy are still not clear enough. Thus, this study aimed to determine the effect of a high-cholesterol diet (HCD) inducing NAFLD on lipolytic gene expression, liver function, lipid profile, and antioxidant enzymes in rabbits and the modulatory effects of probiotic Lactobacillus acidophilus (L. acidophilus) on it. A total of 45 male New Zealand white rabbits, eight weeks old, were randomly divided into three groups of three replicates (5 rabbits/replicate). Rabbits in group I were given a basal diet; rabbits in group II were given a high-cholesterol diet that caused NAFLD; and rabbits in group III were given a high-cholesterol diet as well as probiotics in water for 8 weeks. The results showed that a high-cholesterol diet caused hepatic vacuolation and upregulated the genes for lipoprotein lipase (LPL), hepatic lipase (HL), and cholesteryl ester transfer protein (CETP). Downregulated low-density lipoprotein receptor (LDLr) gene, increased liver enzymes [alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH)], cholesterol, triglycerides (TG), low-density lipoprotein (LDL), glucose, and total bilirubin. On the other hand, it decreased high-density lipoprotein (HDL), total protein, albumin, and liver antioxidants [glutathione peroxidase (GPx), catalase (CAT), reduced glutathione (GSH), and superoxide dismutase (SOD)]. Supplementing with probiotics helped to return all parameters to normal levels. In conclusion, probiotic supplementation, especially L. acidophilus, protected against NAFLD, and restored lipolytic gene expression, liver functions, and antioxidants to normal levels

Ameliorative effects of camel milk and silymarin upon aflatoxin B1 induced hepatic injury in rats

Abstract Aflatoxin B1 (AFB1) poses a major risk to both human and animal health because it contaminates food, feed, and grains. These dangerous effects can be mitigated using natural components. The purpose of this study was to examine the ameliorative effects of camel milk and silymarin supplementation upon aflatoxin B1 induced hepatic injury in rats. This improvement was assessed by measuring leukocytic and deferential counts, serum biochemical parameters, and gene expression of Tumor Necrosis Factor (TNF-α), antioxidant gene (NAD(P)H quinone oxidoreductase 1 (NQO1)), and base excision repair genes (APE1 and OGG1) in the liver tissue, in addition to liver histopathology. Sixty mature males Wister white rats were used to perform the present study; the rats were distributed in six groups (ten rats/group). The control group (without any treatment) received saline by gavage. The camel milk group received 1 ml of camel milk/kg body weight. The silymarin group received 1 ml of silymarin suspension solution at a dose of 20 mg of silymarin/kg of b.wt. The aflatoxin group received an aflatoxin-contaminated diet at a dose of 1.4 mg of aflatoxin /kg of diet and received saline. The camel milk + aflatoxin group received the same previous oral doses of camel milk and an aflatoxin-contaminated diet at the same time. The silymarin + aflatoxin group received the same previous doses of silymarin orally and an aflatoxin-contaminated diet at the same time. The obtained data indicated the deleterious effect of aflatoxin B1 on the leukocytic count, activity of AST and ALT, serum proteins, ferritin, alpha-fetoprotein, carcinoembryonic antigen, liver pathology, and the expression of the studied genes. However, these deleterious effects were mitigated by camel milk and silymarin supplementation. Thus, we could conclude that the ingestion of camel milk and silymarin mitigated the negative effects of AFB1 on the hematology, activity of AST and ALT, serum proteins, ferritin, alpha-fetoprotein, carcinoembryonic antigen, liver pathology, and gene expression in the rat model

Camel milk or silymarin could improve the negative effects that experimentally produced by aflatoxin B1 on rat’s male reproductive system

Abstract Background Camel milk and silymarin have many different beneficial effects on several animal species. Meanwhile, Aflatoxins are mycotoxins with extraordinary potency that pose major health risks to several animal species. Additionally, it has been documented that aflatoxins harm the reproductive systems of a variety of domestic animals. The present design aimed to investigate the impact of aflatoxin B1 (AFB1) on rat body weight and reproductive organs and the ameliorative effects of camel milk and silymarin through measured serum testosterone, testes pathology, and gene expression of tumor necrosis factor (TNF-α), luteinizing hormone receptor (LHR), and steroidogenic acute regulatory protein (StAR) in the testes. A total of sixty mature male Wister white rats, each weighing an average of 83.67 ± 0.21 g, were used. There were six groups created from the rats. Each division had ten rats. The groups were the control (without any treatment), CM (1 ml of camel milk/kg body weight orally), S (20 mg silymarin/kg b. wt. suspension, orally), A (1.4 mg aflatoxin/kg diet), ACM (aflatoxin plus camel milk), and AS (aflatoxin plus silymarin). Results The results indicated the positive effects of camel milk and silymarin on growth, reproductive organs, and gene expression of TNF-α, LHR, and StAR with normal testicular architecture. Also, the negative effect of AFB1 on the rat’s body weight and reproductive organs, as indicated by low body weight and testosterone concentration, was confirmed by the results of histopathology and gene expression. However, these negative effects were ameliorated by the ingestion of camel milk and silymarin. Conclusion In conclusion, camel milk and silymarin could mitigate the negative effect of AFB1 on rat body weight and reproductive organs

Exposure to a Low-Oxygen Environment Causes Implantation Failure and Transcriptomic Shifts in Mouse Uteruses and Ovaries

Hypoxia is a condition in which tissues of the body do not receive sufficient amounts of oxygen supply. Numerous studies have elucidated the intricate roles of hypoxia and its involvement in both physiological and pathological conditions. This study aimed to clarify the impact of a forced low-oxygen environment in early pregnancy by exposing mice to low-oxygen conditions for 24–72 h after fertilization. The treatment resulted in the complete failure of blastocyst implantation, accompanied by vascular hyperpermeability in the uterus. A transcriptome analysis of the uterus revealed remarkable alterations in gene expression between control normoxic- and hypoxic-treatment groups. These alterations were characterized by the differentially expressed genes categorized into the immune responses and iron coordination. Furthermore, exposure to a low-oxygen environment caused apoptosis in the corpus luteum within the ovary and a reduction in progesterone secretion. Consequently, diminished plasma progesterone levels were considered to contribute to implantation failure in combination with the activation of the hypoxic pathway in the uterus. Additionally, previous studies have demonstrated the impact of hypoxic reactions on blastocyst development and the pre-implantation process in the endometrium. Our findings suggest that the corpus luteum exhibits elevated susceptibility to hypoxia, thereby elucidating a critical aspect of its physiological response