Changes in luteal cells distribution, apoptotic rate, lipid peroxidation levels and antioxidant enzyme activities in buffalo (Bubalus bubalis) corpus luteum

Selvaraju, Sellappan; Raghavendra, B. S.; Subramani, Tamilarasan; Priyadharsini, R; Reddy, I. J.; Ravindra, J.P.

doi:10.1016/j.anireprosci.2010.02.017

Cited by 10 publications

(8 citation statements)

References 35 publications

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“…The CL were classified into early (3–5 days, concomitant presence of a regressive CL in the contralateral ovary, Table 1, photo A), mid (6–15 days, Table 1, photo B), late (16–20 days, Table 1, photo C), and regressive (>20 days, Table 1, photo A) based on a modified method previously reported (Selvaraju et al, 2010).…”

Section: Methodsmentioning

confidence: 99%

Immunolocalization, gene expression, and enzymatic activity of cyclooxygenases, prostaglandin e2‐9‐ketoreductase, and nitric oxide synthases in mediterranean buffalo (bubalus bubalis) corpora lutea during diestrus

Parillo

Colella

Maranesi

et al. 2012

Microscopy Res & Technique

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Immunopresence, gene expression, and enzymatic activity of cyclooxygenase 1 (COX1), COX2, PGE2-9-ketoreductase (PGE2-9-K), endothelial (eNOS), and inducible nitric oxide synthases (iNOS), and hormone in vitro production were examined in early, mid, late, and regressive buffalo corpora lutea (CL). COX1 immunosignals were detected in the cytoplasm of small luteal cells, COX2 in large luteal cells, and PGE2-9-K in all luteal cells. COX2 and PGE2-9-K immunosignals were greater in late CL. Immunopresence of both NOS types were evidenced in the nuclei and cytoplasm of all luteal cells, as well as in the nuclei of endothelial cells, during all stages studied. The eNOS and iNOS immunosignals increased during the early stage. COX1 transcripts were lower in late and regressive CL, COX2 in late, PGE2-9-K higher in regressive, and iNOS higher in early and lower in regressive CL. COX1 enzymatic activity was lower in regressive CL, COX2 increased in mid and late stages, and PGE2-9-K was higher in late CL. Endothelial NOS activity was higher during mid and late stages and lower in regressive, whereas iNOS was greater in late and lower in early. Progesterone in vitro release was higher in mid and lower in late phase, while PGF2α synthesis was higher in late CL and lower in regressive, and PGE2 was higher during regressive stage. These results support the idea that COX, NOS, and PGE2-9-K regulate buffalo CL life span. In particular, regressive CL seems involved in the development of the contralateral early CL, through the production of the luteotrophic PGE2.

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Section: Methodsmentioning

confidence: 99%

Immunolocalization, gene expression, and enzymatic activity of cyclooxygenases, prostaglandin e2‐9‐ketoreductase, and nitric oxide synthases in mediterranean buffalo (bubalus bubalis) corpora lutea during diestrus

Parillo

Colella

Maranesi

et al. 2012

Microscopy Res & Technique

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“…Buffalo whole genitalia, containing ovaries with CL at different development stages, were collected immediately after slaughter, during the reproductive period (summer-autumn). The CL, promptly removed, were dissected and classified into early (3-5 days, numerous blood vessels and ovulatory depression), mid (6-15 days, clear neck with ovarian stroma and brownish appearance of surface after decapsulation), and late (16-20 days, fewer blood vessels associated with loss of brownish pigmentation and appearance of the whitish color in CL), based on the method previously reported [10]. Plasma samples were collected by jugulation to confirm the diestrous stages of CL used.…”

Section: Animal Tissue Collectionmentioning

confidence: 99%

Gonadotropin-Releasing Hormone 1 Directly Affects Corpora Lutea Lifespan in Mediterranean Buffalo (Bubalus bubalis) During Diestrus: Presence and In Vitro Effects on Enzymatic and Hormonal Activities1

Zerani

Colella

Maranesi

et al. 2012

Biology of Reproduction

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The expression of gonadotropin-releasing hormone (GNRH) receptor (GNRHR) and the direct role of GNRH1 on corpora lutea function were studied in Mediterranean buffalo during diestrus. Immunohistochemistry evidenced at early, mid, and late luteal stages the presence of GNRHR only in large luteal cells and GNRH1 in both small and large luteal cells. Real-time PCR revealed GNRHR and GNRH1 mRNA at the three luteal stages, with lowest values in late corpora lutea. In vitro corpora lutea progesterone production was greater in mid stages and lesser in late luteal phases, whereas prostaglandin F2 alpha (PGF2alpha) increased from early to late stages, and PGE2 was greater in the earlier-luteal phase. Cyclooxygenase 1 (prostaglandin-endoperoxide synthase 1; PTGS1) activity did not change during diestrus, whereas PTGS2 increased from early to late stages, and PGE2-9-ketoreductase (PGE2-9-K) was greater in late corpora lutea. PTGS1 activity was greater than PTGS2 in early corpora lutea and lesser in late luteal phase. In corpora lutea cultured in vitro, the GNRH1 analog (buserelin) reduced progesterone secretion and increased PGF2alpha secretion as well as PTGS2 and PGE2-9-K activities at mid and late stages. PGE2 release and PTGS1 activity were increased by buserelin only in late corpora lutea. These results suggest that GNRH is expressed in all luteal cells of buffalo, whereas GNRHR is only expressed in large luteal phase. Additionally, GNRH directly down-regulates corpora lutea progesterone release, with the concomitant increases of PGF2al-pha production and PTGS2 and PGE2-9-K enzymatic activities.buffalo, corpus luteum, gonadotropin-releasing hormone 1 (GNRH1), progesterone, prostaglandin F2alpha

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“…Steroidogenesis is considered an important source of ROS production in the corpus luteum. However, there are high levels of antioxidant enzymes in the corpus luteum including catalase, SOD, and glutathione peroxidase, which protect luteal cells against oxygen radicals produced during steroidogenesis [ 64 ]. It has been reported that SOD protects the corpus luteum against superoxide radicals to stimulate the luteal cells for the production of progesterone [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Ginseng alleviates folliculogenesis disorders via induction of cell proliferation and downregulation of apoptotic markers in nicotine-treated mice

et al. 2022

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Background Ginseng is a powerful phytoestrogen with high antioxidant properties. Objective This study aimed to evaluate the effect of Panax Ginseng (PG) on folliculogenesis, proliferation, and apoptosis in the ovary impaired by nicotine. Methods Forty adult mice were divided into five groups. Control, sham, and nicotine groups, and co-treated groups of nicotine and ginseng in doses of 0.5 and 1 g/kg. Folliculogenesis was assessed via histopathology and serum evaluation of estradiol, progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) by ELISA. Lipid peroxidation and antioxidant enzyme activities both in homogenate tissue and serum were assayed by colorimetric analysis. Apoptotic markers of cytochrome c (Cyt c), Bax, and Bcl-2 were evaluated by RT-PCR. Proliferative index was studied by the Ki-67 immunostaining procedure. Results In comparison to the control or sham groups, nicotine significantly reduced the levels of FSH, LH, and estradiol hormones. An insignificant reduction was observed in the progesterone hormone. Nicotine reduced all healthy follicle numbers, except primordial (P = 0.001). Malondialdehyde (MDA) was increased in tissue and serum in the nicotine group (P = 0.01). Serum catalase (CAT) and enzymatic activity of superoxide dismutase (SOD) both were reduced in tissue and the serum, in the nicotine group. Nicotine induced a reduction in the proliferative indexes of granulosa and theca cells in pre-antral and antral follicles (P = 0.001). However, its effect on the proliferative index of stroma cells was not significant. Apoptotic markers were elevated in the nicotine group (P = 0.001). Co-treatment with ginseng elevated all sex hormones, increased healthy follicles, and reduced tissue or serum lipid peroxidation, compared with the nicotine group (p < 0.05). Co-Treatment with ginseng also reduced the expression of apoptotic markers and increased the proliferative indexes in granulosa and theca cells in pre-antral and antral follicles and also in stroma cells, in comparison to the nicotine group (P = 0.001). All above-mentioned alterations following treatment with ginseng were remarkable, especially in the dose of 1 g/kg. Conclusion This study showed ginseng protects folliculogenesis via alteration of hypothalamic- pituitary–gonadal (HPG) axis, induction of proliferation in ovarian somatic cells, reduction of lipid peroxidation, and downregulation of apoptotic markers in the mouse ovary, treated with nicotine.

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Changes in luteal cells distribution, apoptotic rate, lipid peroxidation levels and antioxidant enzyme activities in buffalo (Bubalus bubalis) corpus luteum

Cited by 10 publications

References 35 publications

Immunolocalization, gene expression, and enzymatic activity of cyclooxygenases, prostaglandin e2‐9‐ketoreductase, and nitric oxide synthases in mediterranean buffalo (bubalus bubalis) corpora lutea during diestrus

Immunolocalization, gene expression, and enzymatic activity of cyclooxygenases, prostaglandin e2‐9‐ketoreductase, and nitric oxide synthases in mediterranean buffalo (bubalus bubalis) corpora lutea during diestrus

Gonadotropin-Releasing Hormone 1 Directly Affects Corpora Lutea Lifespan in Mediterranean Buffalo (Bubalus bubalis) During Diestrus: Presence and In Vitro Effects on Enzymatic and Hormonal Activities1

Ginseng alleviates folliculogenesis disorders via induction of cell proliferation and downregulation of apoptotic markers in nicotine-treated mice

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