Vitamin D3 regulates apoptosis and proliferation in the testis of D-galactose-induced aged rat model

Abstract The age-associated imbalances between proliferation and apoptosis lead to impaired spermatogenesis and infertility. The age-associated decline in vitamin D3 levels has been reported and suggested the anti-aging potential of vitamin D3. However, the age-associated decline levels of vitamin D3 has not been studied in relation to the testicular activity. Thus, we investigated the effect of vitamin D3 on the expression of testicular proliferation markers, apoptotic markers, antioxidants system and oxidative stress in a D-gal-induced aged rat model. The present study investigated the levels of vitamin D3 and AGE in serum and testes along with the expression of the AGE-receptor (AGER) in the testis. Vitamin D3 treatment significantly increases cell proliferation and decreases apoptosis in a D-gal-induced aged rat testis. Furthermore, vitamin D3 significantly decreases oxidative stress in aged rat testis by improving the antioxidant defense systems. The expression of AGER was down-regulated by vitamin D3 treatment in aged testis. The circulating and intra-testicular AGE was higher in aged groups, however, only circulating vitamin D3 levels decreased in aged groups. The immunolocalization of VDR showed increased immunostaining in the testis by vitamin D3 treatment. Thus, it can be concluded that vitamin D3 delays testicular senescence by regulating proliferation and apoptosis.

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Changes in Bone Metabolism and Antioxidant Defense Systems in Menopause-Induced Rats fed Bran Extract from Dark Purple Rice (Oryza sativa L. Cv. Superjami)

Nutrients ◽

10.3390/nu13092926 ◽

2021 ◽

Vol 13 (9) ◽

pp. 2926

Author(s):

Soo Im Chung ◽

Su Noh Ryu ◽

Mi Young Kang

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Bone Loss ◽

Bone Metabolism ◽

Rice Bran ◽

Antioxidant Defense ◽

Control Group ◽

Defense Systems ◽

Antioxidant Defense Systems ◽

And Oxidative Stress

Menopause is a matter of concern for women’s health due to a deficiency of female hormones; additionally, reactive oxygen species and aging can cause osteoporosis. Food becomes increasingly interesting as a menopausal woman’s alternative to hormone therapy. The effects of ethanol extracts from dark purple Superjami rice bran on bone metabolism and antioxidant defense systems in menopause-induced animal models were evaluated. Female rats underwent sham surgery or were ovariectomized to induce a menopause-like state. Rats were divided into a sham control group (SHAM), an ovariectomized control group (OVX), and an ovariectomized grou supplemented with Superjami rice bran extract group (OVX-S) and fed for 8 weeks. The OVX groups exhibited significantly more weight gain, amounts of bone turnover biochemical markers (alkaline phosphatase, osteocalcin, and C-terminal telopeptide), bone loss, lipid-peroxidation and oxidative stress than the SHAM group. However, Superjami bran extract added to the diet resulted in a significant reduction in body weight and lipid peroxidation, as well as enhanced bone metabolism and antioxidant enzyme activities, in ovariectomized rats. These results propound that extracts from Superjami rice bran have therapeutic potentiality against bone loss and oxidative stress in menopause-induced states and will be useful in preventing postmenopausal osteoporosis and oxidative damage.

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Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death

Experimental Biology and Medicine ◽

10.1177/1535370221995207 ◽

2021 ◽

pp. 153537022199520

Author(s):

Nanees F El-Malkey ◽

Amira E Alsemeh ◽

Wesam MR Ashour ◽

Nancy H Hassan ◽

Husam M Edrees

Keyword(s):

Oxidative Stress ◽

Rat Model ◽

Intestinal Ischemia ◽

Ischemia Reperfusion ◽

Protective Role ◽

Beclin 1 ◽

Male Rats ◽

Fetuin A ◽

Intestinal Ischemia Reperfusion ◽

And Oxidative Stress

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

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