http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Al-Ajmi, Nada,Al-Maghrebi, May,Renno, Waleed Mohammed The Korean Society of Pharmacology 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.4
The anti-apoptotic effect of (-)-epigallocatechin-3-gallate (EGCG) during unilateral testicular torsion and detorsion (TT/D) was established in our previous study. In mice, the smallest inhibitor of apoptosis, survivin, is alternatively spliced into three variants, each suggested to have a unique function. Here, we assessed how EGCG exerts its protective effect through the expression of the different survivin splice variants and determined its effect on the morphology of the seminiferous tubules during TT/D. Three mouse groups were used: sham, TT/D+vehicle and TT/D treated with EGCG. The expression of the survivin variants (140 and 40) and other apoptosis genes (p53, Bax and Bcl-2) was measured with semi-quantitative RT-PCR. Histological analysis was performed to assess DNA fragmentation, damage to spermatogenesis and morphometric changes in the seminiferous tubules. In the TT/D+vehicle group, survivin 140 expression was markedly decreased, whereas survivin 40 expression was not significantly different. In parallel, there was an increase in the mRNA level of p53 and the Bax to Bcl-2 ratio in support of apoptosis induction. Histological analyses revealed increased DNA fragmentation and increased damage to spermatogenesis associated with decreased seminiferous tubular diameter and decreased germinal epithelial cell thickness in the TT/D+vehicle group. These changes were reversed to almost sham levels upon EGCG treatment. Our data indicate that EGCG protects the testis from TT/D-induced damage by protecting the morphology of the seminiferous tubules and modulating survivin 140 expression.
Nada Al-Ajmi,May Al-Maghrebi,Waleed Mohammed Renno 대한약리학회 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.4
The anti-apoptotic effect of (-)-epigallocatechin-3-gallate (EGCG) during unilateral testicular torsion and detorsion (TT/D) was established in our previous study. In mice, the smallest inhibitor of apoptosis,survivin, is alternatively spliced into three variants, each suggested to have a unique function. Here,we assessed how EGCG exerts its protective effect through the expression of the different survivin splice variants and determined its effect on the morphology of the seminiferous tubules during TT/D. Three mouse groups were used: sham, TT/D+vehicle and TT/D treated with EGCG. The expression of the survivin variants (140 and 40) and other apoptosis genes (p53, Bax and Bcl-2) was measured with semi-quantitative RT-PCR. Histological analysis was performed to assess DNA fragmentation,damage to spermatogenesis and morphometric changes in the seminiferous tubules. In the TT/D+vehicle group, survivin 140 expression was markedly decreased, whereas survivin 40 expression was not significantly different. In parallel, there was an increase in the mRNA level of p53 and the Bax to Bcl-2 ratio in support of apoptosis induction. Histological analyses revealed increased DNA fragmentation and increased damage to spermatogenesis associated with decreased seminiferous tubular diameter and decreased germinal epithelial cell thickness in the TT/D+vehicle group. These changes were reversed to almost sham levels upon EGCG treatment. Our data indicate that EGCG protects the testis from TT/D-induced damage by protecting the morphology of the seminiferous tubules and modulating survivin 140 expression.
Gardinal, R.,Calomeni, G.D.,Consolo, N.R.B.,Takiya, C.S.,Freitas, J.E. Jr,Gandra, J.R.,Vendramini, T.H.A.,Souza, H.N.,Renno, F.P. Asian Australasian Association of Animal Productio 2017 Animal Bioscience Vol.30 No.1
Objective: Two experiments were performed to evaluate the effects of coated slow-release urea on nutrient digestion, ruminal fermentation, nitrogen utilization, blood glucose and urea concentration (Exp 1), and average daily gain (ADG; Exp 2) of steers. Methods: Exp 1: Eight ruminally fistulated steers [$503{\pm}28.5kg$ body weight (BW)] were distributed into a d $4{\times}4$ Latin square design and assigned to treatments: control (CON), feed grade urea (U2), polymer-coated slow-release urea A (SRA2), and polymer-coated slow-release urea B (SRB2). Dietary urea sources were set at 20 g/kg DM. Exp 2: 84 steers ($350.5{\pm}26.5kg$ initial BW) were distributed to treatments: CON, FGU at 10 or 20 g/kg diet DM (U1 and U2, respectively), coated SRA2 at 10 or 20 g/kg diet DM (SRA1 and SRA2, respectively), and coated SRB at 10 or 20 g/kg diet DM (SRB1 and SRB2, respectively). Results: Exp 1: Urea treatments (U2+SRA2+SRB2) decreased (7.4%, p = 0.03) the DM intake and increased (11.4%, p<0.01) crude protein digestibility. Coated slow-release urea (SRA2+-SRB2) showed similar nutrient digestibility compwared to feed grade urea (FGU). However, steers fed SRB2 had higher (p = 0.02) DM digestibility compared to those fed SRA2. Urea sources did not affect ruminal fermentation when compared to CON. Although, coated slow-release urea showed lower (p = 0.01) concentration of $NH_3-N$ (-10.4%) and acetate to propionate ratio than U2. Coated slow-release urea showed lower (p = 0.02) urinary N and blood urea concentration compared to FGU. Exp 2: Urea sources decreased (p = 0.01) the ADG in relation to CON. Animals fed urea sources at 10 g/kg DM showed higher (12.33%, p = 0.01) ADG compared to those fed urea at 20 g/kg DM. Conclusion: Feeding urea decreased the nutrient intake without largely affected the nutrient digestibility. In addition, polymer-coated slow-release urea sources decreased ruminal ammonia concentration and increased ruminal propionate production. Urea at 20 g/kg DM, regardless of source, decreased ADG compared both to CON and diets with urea at 10 g/kg DM.