Proliferating Cell Nuclear Antigen Immunoreactivity Research Articles

Caffeic acid phenethyl ester attenuates Enterococcus faecalis infection in vivo: antioxidants and NF-κB have a protective role against stomach damage.

The mammalian gastrointestinal tract hosts a significant microbial symbiont community, an intriguing feature of this complex organ system. This study aimed to investigate the anti-inflammatory, antioxidant, and protective effects of caffeic acid phenethyl ester (CAPE) against Enterococcus faecalis infection in the stomach at a dose of 106 CFU in Swiss mice. A total of 30 mice were randomly assigned to three groups of ten mice each. Group I was the negative control, Group II was infected orally with E. faecalis for 18 days, and Group III was infected with E. faecalis and treated with CAPE orally at a daily dose of 4 mg/kg for 18 days. We assessed the antioxidant activities of stomach homogenate and the immunohistochemical expressions of the transcription factor nuclear factor kappa B (NF-κB) and proliferating cell nuclear antigen (PCNA). Histopathological examination was performed on the stomachs of all mice. Group II had decreased levels of antioxidant activity and positive expressions of NF-κB and PCNA. Histological observations revealed an increase in mucosal and glandular thickness compared with Group I. Group III, treated with CAPE, showed a significant increase in antioxidant activities and a significant decrease in NF-κB and PCNA immunoreactivities compared with Group II. In addition, Group III showed restoration of the normal thickness of the non-glandular and glandular parts of the stomach. Our results revealed that E. faecalis infection has damaging effects on the stomach and proved that CAPE has promising protective, anti-inflammatory, and antioxidant effects against E. faecalis. Further studies may investigate the potential therapeutic effects of CAPE against E. faecalis infection.

Rosuvastatin and diosmetin inhibited the HSP70/TLR4 /NF-κB p65/NLRP3 signaling pathways and switched macrophage to M2 phenotype in a rat model of acute kidney injury induced by cisplatin

Numerous efforts to manage acute kidney injury (AKI) were unsuccessful because its pathophysiology is still poorly understood. Thus, our research hotspot was to explore the possible renoprotective effects of rosuvastatin (Ros) and diosmetin (D) on macrophage polarization and the role of HSP70/TLR4/MyD88/NF-κB p65/NLRP3/STAT3 signaling in cis-induced AKI and study the activity of D against uropathogenic bacteria. Fifty-four albino male rats were randomized into 9 groups equally: Control, Ros, D20, D40, untreated Cis, and Cis groups cotreated with Ros, D20, D40 and Ros+D40 for 10 days. Our results indicated that Ros and D, in a dose-dependent manner, markedly restored body weight, systolic blood pressure, and renal histological architecture besides significantly upregulated SOD levels, expression of anti-inflammatory CD163 macrophages, arginase1levels, IL-10 levels,STAT3 and PCNA immunoreactivity. Also, they significantly downregulated renal index, serum urea, serum creatinine, serum cystatin c, inflammatory biomarkers (C reactive protein, IL1β & TNF-α), MDA levels, HSP70/TLR4/MyD88/NF-κB p65/NLRP3 expressions, proinflammatory CD68 macrophages and caspase-3 immunoreactivity, resulting in a reversal of cis-induced renal damage. These findings were further confirmed by molecular docking that showed the binding affinity of Ros and D towards TLR4 and NLRP3. Furthermore, D had antibacterial action with a minimum inhibitory concentration ranging from 128 to 256 µg/mL and caused a delay in the growth of the tested isolates, and negatively affected the membrane integrity. In conclusion, Ros and D had antioxidant, anti-inflammatory and antiapoptotic properties and switched macrophage from proinflammatory CD68 to anti-inflammatory CD163. Additionally, the targeting of HSP70/TLR4/MyD88/NF-κB p65/NLRP3/STAT3 signals are effective therapeutic strategy in AKI.

Protective effects of hesperidin in gastric damage caused by experimental ischemia-reperfusion injury model in rats.

This study evaluated the protective effect of hesperidin on injury induced by gastric ischemia-reperfusion. Fifty male Sprague Dawley rats (250-300g) were divided into five groups: control (C), sham (S), ischemia (I), ischemia-reperfusion (I/R) and hesperidin + ischemia-reperfusion (Hes + I/R). Hesperidin was injected intraperitoneally at the dose of 100mg/kg one hour before the experimental stomach ischemia-reperfusion. Celiac artery was ligated. After 45minutes ischemia and 60minutes reperfusion period, blood samples were obtained under anesthesia. Then, animals were sacrificed, stomach tissues were excised for biochemical, and histopathological analyses were performed. Malondialdehyde levels and superoxide dismutase, glutathione peroxidase activities and total antioxidant status (TAS), total oxidant status (TOS), protein, total thiol parameters were measured in plasma, and tissue homogenate samples. H + E, periodic acid-Schiff, hypoxia inducible factor, terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end-labeling (TUNEL), and proliferating cell nuclear antigen (PCNA) for cell proliferation as immunohistochemical parameters were determined. Upon biochemical and histopathological assessment, hesperidin decreased stomach tissue changes in comparison with IR group. Ischemia-reperfusion injury led to a considerably increase in malondialdehyde, protein, and TOS levels (p < 0.001) in stomach tissue. Hesperidin treatment significantly decreased malondialdehyde, protein, and TOS levels (p < 0.001). Hesperidin increased superoxide dismutase, TAS, total thiol and glutathione peroxidase activities in comparison with IR group. Hesperidin reduced damage and also increased TUNEL and PCNA immunoreactivity in stomach tissue. Hesperidin was able to decrease I/R injury of the stomach tissue due to inhibition of lipid peroxidation and protein oxidation, duration of antioxidant, and free radical scavenger properties. Consequently, hesperidin can provide a beneficial therapeutic choice for preventing stomach tissue ischemia-reperfusion injury in clinical application.

The amelioration of ovarian dysfunction by hesperidin in malathion-treated mice through the overexpression of PCNA and FSHR proteins

ObjectiveMalathion (MAL), a pesticide used for decades, is a highly toxic substance. Several studies have documented the negative effects of such agents on reproductive organ physiology, but the precise mechanism of action in the induction of ovarian dysfunction remains unclear. Therefore, the purpose of this research was to examine the effects of the antioxidant hesperidin (HES) on ovarian damage and toxicity caused by malathion. Materials and methodsIn this experiment, forty adult female bulb/c mice weighing 27–30 g were categorized into four groups, namely hesperidin (20 mg/kg, i.p.), malathion (3 mg/kg, i.p.), malathion + hesperidin, and control groups. Following a period of 35 consecutive days of treatment, mice were euthanized, and their ovarian tissues were gathered for the purposes of histopathological analysis by H&E staining, immunohistochemical assessment via proliferating cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSHR) immunostaining, and biochemical evaluation via measuring the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β). In addition, serum samples were collected from the blood of mice to perform hormonal analyses, especially 17β-estradiol (E2), progesterone (P4), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). ResultsThe results demonstrated that MAL exposure resulted in the development of abnormalities in the architecture and structure of ovaries. Also, the treatment of mice with MAL led to declined follicular counts at all three stages, namely, primary, secondary, and tertiary, reduced serum levels of sex hormones, decreased immunoreactivity of FSHR and PCNA, and diminished activity of CAT and SOD enzymes. In contrast, it caused an increase in MDA, IL-1β, and TNF-α, as well as the count of atretic follicles. Nonetheless, it was observed that HES exhibited the ability to ameliorate the deleterious impacts of malathion across all the aforementioned parameters. ConclusionTreatment with HES via upregulating the protein expression of PCNA and FSHR and activating antioxidant defense was able to ameliorate the adverse effects of MAL on ovarian tissues.

Anti-inflammatory, anti-apoptotic, and antioxidant effects of obestatin on the colonic mucosa following acetic acid-induced colitis.

Cellular inflammatory processes, fibrogenesis, and apoptosis are the most characteristic pathologic features of colonic injury and colitis in human and experimental animals. Obestatin, a peptide derived from proghrelin, is reported to have significant protective and curative actions on many gastrointestinal tract inflammatory diseases, including ulcerative colitis. However, its exact protective mechanisms and the associated histopathological changes, are still in need of deeper exploration. This study explores the effect of obestatin on the course of acetic acid (AA)-induced colitis as an antifibrotic, anti-inflammatory, and anti-apoptotic agent in relation to associated tissue stress parameters. A total of 40 healthy male albino Wistar rats weighing 200-250 g were recruited in this study. The rats were classified into four groups (10 rats each); group I: control, group II: obestatin only treated (16 nmol/kg), group III: colitis induced group (AA 1 mL of 3.5% (v/v), and group IV: AA-induced colitis + obestatin for 14 days. Colonic samples were examined after staining haematoxylin and eosin, Alcian blue, Masson trichrome. The expression of proliferating cell nuclear antigen (PCNA), nuclear factor kappa B (NFkB), and caspase-3 was estimated after immunohistochemical staining. Oxidative stress parameters, antioxidant enzymes, tissue myeloperoxidase (MPO) activity, ghrelin, and fibrogenesis markers were identified by immunoassay and colorimetric techniques. Colonic mucosa of group IV exhibited mucosal healing and regeneration of the surface epithelium with the restoration of the goblet cells' function together with a decline in PCNA, NFkB, and caspase-3 immunoreactivity in comparison to group III. This was accompanied by a reduction of the expression of fibrosis markers, hydroxyproline and fibronectin. In addition, tissue antioxidant status was significantly improved with a marked reduction of tissue MPO. Ghrelin level was significantly increased in comparison to group III. Group IV exhibited significant reduction in the levels of oxidative stress markers, malondialdehyde, total oxidant status with a marked increase in the activity of antioxidant enzymes, superoxide dismutase, catalase, and total cellular total antioxidant capacity. The concomitant treatment of obestatin inhibits the development of AA-induced colitis. The data signify that it has both curative and protective effects via antifibrotic, antioxidant, and anti-inflammatory activities.

Canagliflozin alleviates experimentally induced benign prostate hyperplasia in a rat model: exploring potential mechanisms involving mir-128b/EGFR/EGF and JAK2/STAT3 signaling pathways through in silico and in vivo investigations

Benign prostatic hyperplasia (BPH) poses a significant health concern amongst elderly males. Canagliflozin (Cana), a selective sodium-glucose co-transporter 2 (SGLT2) inhibitor, has a powerful anti-inflammatory influence. Nevertheless, its role in treating BPH has not been clarified. Therefore, the study aimed to investigate the potential ameliorative effect of Cana on experimentally induced BPH in rats and explore the underlying mechanisms compared to the standard finasteride (Fin). The study employed histological analysis, biochemical assays using ELISA, and western blotting. Animals were categorized into four groups: Control (2.5 ml/kg CMC, orally + 3 ml/kg olive oil, subcutaneous), BPH (3 mg/kg testosterone, subcutaneous + CMC orally), Fin-treated BPH (5 mg/kg, orally), and Cana-treated BPH (5 mg/kg, orally), for 28 days. The BPH group showed obvious BPH manifestations including an increase in prostate weight (PW), prostate index (PI), dihydrotestosterone (DHT) level, and histological aberrations compared to control. Fin and Cana therapy had a comparable impact. Cana treatment significantly reduced PW and PI, besides it improved prostatic biochemical, and histopathological features compared to BPH, consistent with in silico study findings. Cana was associated with downregulation of the androgen axis, increased miR-128b expression, with a lowered expression of epidermal growth factor (EGF) and its receptor. Phosphorylation of STAT3 and its downstream proliferative markers were significantly reduced suggesting apoptotic activity. Cana markedly rescued the BPH-induced upregulation of IL-1β, and iNOS levels. Altogether, the current study demonstrates that Cana could impede BPH progression, possibly by modulating miR-128b/EGFR/EGF and JAK2/STAT3 pathways and downregulating AR, cyclin D1, and PCNA immunoreactivity.

RETRACTED: Exercise ameliorates hippocampal damage induced by Wi-Fi radiation; a biochemical, histological, and immunohistochemical study

IntroductionNowadays, using electromagnetic devices (EMD) has been increased. However, the control of EMD hazards was poorly evaluated, especially those affected the hippocampus. Regular physical exercises are safe, easily, inexpensive, and acceptable for long-term use. It is reported that exercise protects against many health problems. Aimis to investigate the hypothesis of the possible prophylactic effect of exercise on the hippocampal damage induced by electromagnetic waves of Wi-Fi. Material and methodsAdult male albino rats were divided into four groups: group I (control), group II (exercise), group III (Wi-Fi), and group IV (exercise -Wi-Fi). Hippocampi were subjected to biochemical, histological, and immunohistochemical techniques. ResultsIn group III, a significant increase in the oxidative enzymes as well as decrease in antioxidant enzymes were detected in rat hippocampus. Additionally, the hippocampus showed degenerated pyramidal and granular neurons. An evident decrease in both PCNA and ZO-1 immunoreactivity was also noticed. In group IV, physical exercise alleviates the effect of Wi-Fi on previously mentioned parameters. ConclusionRegular physical exercise performance significantly minimizes the hippocampal damage and protects against the hazarders of chronic Wi-Fi radiation exposure.

Immunohistochemical Evidence of Melatonin Protection on Lung Tissue During Chemotherapy

The present study investigated the possible protective effects of melatonin on Bleomycin, Cisplatin and etoposide (BEP) chemotherapy regimens using immunohistochemistry. Forty male Wistar rats were divided into four groups of ten as; group 1 as untreated control; group 2 as BEP group which received the three cycles of 21 days’ regimen each of 0.5¥ dose levels ofBEP (bleomycin 0.75 mg/kg, etoposide 7.5 mg/kg and cisplatin 1.5 mg/kg). Rats in the group 3 (MEL group) received 10 mg/kg/day melatonin once daily. Group 4 received the melatonin (30 min before the BEP injections) and BEP as in groups 2. Proliferating cell nuclear antigen (PCNA) staining was used to detect cell proliferation and caspase-3, caspase-9 and Caspase-8 were detected to investigate apoptosis. PCNA immunostaining in alveolar epithelium, alveolar macrophages and bronchus was weak to moderate in BEP group. However, diffuse and strong caspase immunoreactions for caspase-3, caspase 8- and caspase-9 were detected in the bronchioles epithelium, vascular endothelium, alveolar luminal macrophages in the BEP group. PCNA and caspase immunoreactivities in MEL and Mel + BEP groups were close to the control one. The surface are in the BEP group was significantly reduced as compared to the control one ((P<0.05). However, in MEL and Mel + BEP groups, it was close to the control value (P>0.05). It can be concluded that BEP regimen can affects negatively on lung tissue and melatonin inhibits lung tissue injuries during BEP chemotherapy.

Possible protective and curative effects of selenium nanoparticles on testosterone-induced benign prostatic hyperplasia rat model.

Men over the age of 40 are more likely to develop benign prostatic hyperplasia (BPH). BPH is characterised by proliferation of the prostatic epithelium and stroma. Selenium in the form of nanoparticles is an essential metalloid mineral and antioxidant. In this study, selenium nanoparticles (SeNPs) were tested for their potential protective and curative impacts on BPH in rats. Fifty male Sprague-Dawley rats were randomly divided into five groups: Group I (Control group); Group II (Orchiectomised group): bilateral orchiectomy was conducted on rats; Group III (BPH group): testosterone (TE) enanthate injection was used to induce BPH; Group IV (Protective group): rats were given SeNPs before subjecting rats to BPH; Group V (Curative group): rats were succumbed to BPH, followed by administration of SeNPs. Measurement of prostate specific antigen (PSA) and TE in serum was performed and prostates were weighed and prepared for histological, immunohistochemical and ultrastructural examination. In the BPH group, serum TE and PSA levels, as well as prostate weight, increased significantly and significant decreases were observed in the protective and curative groups. Reduced acinar lumen, expansion of stroma and epithelial hyperplasia were noticed in the BPH group, which were ameliorated significantly in both the protective and curative groups. There was an increase in proliferating cell nuclear antigen immunoreaction in the BPH group and a decrease in both the protective and curative groups. On transmission electron microscopy of BPH group, the nuclei appeared irregular with dilated endoplasmic reticulum, loss of cell boundaries and apical microvilli. The protective group showed more improvement than the curative group. The effects of SeNPs on BPH induced by TE in rats, were both protective and curative, although the protective effects were more pronounced.

The potential therapeutic efficacy of intravenous versus subconjunctival mesenchymal stem cells on experimentally ultraviolet-induced corneal injury in adult male albino rats.

The X-rays and the visible light are the main source of ultraviolet radiation (UVR). About 90% of ultraviolet B (UVB) is absorbed by the cornea which may promote corneal inflammation, oedema and damage of its epithelial layer. Bone marrow mesenchymal stem cells (BM-MSCs) have been demonstrated to ameliorate the injured corneal tissue and accelerate its wound healing. This study aimed to compare the healing effect of intravenous (IV) versus subconjunctival (SC) BM-MSCs on the rats' corneas subjected to UVB-irradiation. Ten rats were used as donors for BM-MSCs and the other 40 were allocated into four equal groups: group I (control group), group II (ultraviolet-irradiated group), group III (ultraviolet-irradiated + IV BM-MSCs-treated group) and group IV (ultraviolet-irradiated +SC BM-MSCs-treated group). Rats of all groups were euthanized after 3 weeks and the corneal specimens were processed for histopathological, immunohistochemical and electron microscopy assessment. Ultraviolet-irradiated group showed remarkable thinning of epithelial thickness, wide partial epithelial separation, and desquamation. Neovascularisation of the disorganised stroma and disrupted Descemet's membrane were observed. The superficial and basal epithelial cells appeared irregular and separated by wide intercellular spaces and inflammatory cells. Immunohistochemical examination showed a significant decrease in proliferating cell nuclear antigen immunoreaction. In contrast, minimal changes were observed in rats treated with BM-MSCs with more improvement associated with the subconjunctival administration compared to IV route. Local SC injection of BM-MSCs has an amazing regenerative efficacy on the corneal injury compared to the systemic IV route.

Oogenesis and expression of PCNA and vitellogenin in Geophagus native to the Amazon basin in pre- and post-hydroelectric dam periods

Oogenesis in fish is a process that involves cell proliferation, growth and maturation. In rivers blocked by hydroelectric dams, these factors can be altered and affect the reproduction mechanism of the species. Regarding this scenario, the present study aimed to describe oogenesis in two cichlids native to the Amazon basin, Geophagus argyrostictus and G. altifrons, during pre- and post-dam periods of the Xingu River. Females of both Geophagus species were captured and biometric measurements were taken. Afterwards, the fish were euthanized, and the gonads were removed and subjected to histological processing for light microscopy, scanning electron microscopy and immunoperoxidase staining. Oocyte diameter and zona radiata thickness were also measured. The ovaries appeared in pairs, where according to their shape, size, vascularization and cell organization, five stages were described for both species. In the post-dam period, there was a reduction in the mean diameter of the oocytes, especially type IV, and a decrease in the thickness of the zona radiata, mainly, in G. argyrostictus. In both species, there was a greater presence of oocyte atresia in the post-dam period. PCNA immunoreactivity was more intense in type I and II oocytes, while vitellogenin immunoreactivity occurred in the cytoplasm and follicular cells of oocytes III and IV. These data suggest that because of changes in the level/flow of the river, the gonads of these two species adjust to the new environment, with a decrease in mean diameter and zona radiata thickness of the oocytes, which can interfere with the reproduction of the animals.

Glyphosate, AMPA and glyphosate-based herbicide exposure leads to GFAP, PCNA and caspase-3 increased immunoreactive area on male offspring rat hypothalamus.

Glyphosate, aminomethylphosphonic acid (AMPA), and glyphosate-based herbicides altered the neuroendocrine axis, the content of brain neurotransmitters, and behavior in experimental animal models. Glyphosate alone, AMPA or Roundup® Active were administered to postpartum female rats, from P0 to P10, and their water consumption was measured daily. The immunoreactivity for glial fibrillary acidic protein (GFAP), proliferating cell nuclear antigen (PCNA) and caspase-3 was measured in the anterior, medial preoptic, periventricular, supraoptic and lateroanterior hypothalamic nuclei of P0-P10 male pups after exposure, via lactation, to these xenobiotics. Puppies exposed to glyphosate had a moderate level of GFAP with no overlapping astrocyte processes, but this overlapping was observed after Roundup® Active or AMPA exposure. After being exposed to Roundup® Active or AMPA, PCNA-positive cells with strong immunoreactivity were found in some hypothalamic nuclei. Cells containing caspase-3 were found in all hypothalamic nuclei studied, but the labeling was stronger after Roundup® Active or AMPA exposure. Xenobiotics significantly increased the immunoreactivity area for all of the markers studied in the majority of cases (p<0.05). AMPA or Roundup® Active treated animals had a greater area of PCNA immunoreactivity than control or glyphosate alone treated animals (p<0.05). The effects observed after xenobiotic exposure were not due to increased water intake. The increased immunoreactivity areas observed for the markers studied suggest that xenobiotics induced a neuro-inflammatory response, implying increased cell proliferation, glial activation, and induction of apoptotic pathways. The findings also show that glyphosate metabolites/adjuvants and/or surfactants present in glyphosate commercial formulations had a greater effect than glyphosate alone. In summary, glyphosate, AMPA, and glyphosate-based herbicides altered GFAP, caspase-3, and PCNA expression in the rat hypothalamus, altering the neuroendocrine axis.

Caffeic acid abrogates amyloidosis, hypospermatogenesis and cell membrane alterations in the testes and epididymis of fructose-diabetic rats by upregulating steroidogenesis, PCNA and Nrf2 expression

The fructose-streptozotocin (FRU-STZ) diabetic model has been presented as a viable model of type2 diabetes but its impact on the testes and epididymis of Wistar rats is yet to be investigated. In this study, we probed the role of caffeic acid, a potent antioxidant, in FRU-STZ diabetic rats. Twenty normoglycemic rats were randomly divided into four groups of five rats each: Control, Fructose-Streptozotocin (FRU+STZ), Fructose-Streptozotocin + Caffeic Acid (FRU+STZ+CA), and Caffeic Acid (CA). Diabetes was induced by the administration of 10 % fructose solution ad libitum for 2 weeks followed by a single intraperitoneal injection of 50 mg/kg bwt of streptozotocin. Treatment with CA (50 mg/kg bwt) lasted for two weeks. Results showed that FRU-STZ diabetes was able to induce amyloidosis and histopathological deficits in the testis and epididymis characteristic of cytotoxic agents. Poor PCNA immunoreactivity, reactive Nrf2 expression, and defective steroidogenesis were also observed in the diabetic group. FRU-STZ diabetes was also associated with significantly increased Na+-K+ ATPase activity in both testes and epididymis. Treatment with caffeic acid was able to restore steroidogenesis and spermatogenesis in the diabetic rats to levels comparable to the control; histological features and Na+-K+ ATPase activity were also reduced in the CA-treated group. Generally, normal rats treated with caffeic acid did not evince any deleterious effects. Our study demonstrates that CA exerts a protective role in FRU-STZ diabetes.

Effects of neferine on retinal tissue in experimental diabetic rat model.

To investigate vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) immunoreactivities, as well as apoptosis and oxidative stress levels in Streptozotocin (STZ)-induced diabetic rats, and determine how neferine affected these parameters. Thirty-five male Sprague Dawley rats were divided into five groups of seven. Fasting blood glucose was measured 72h after diabetes mellitus (DM) induction in 21 rats using 60mg/kg STZ dissolved in 0.4ml (0.1M) sodium-citrate buffer (pH:4.5), with values > 250mg/dl considered diabetic. Group 1 received no treatment. Group 3 (healthy rats) received daily intraperitoneal (IP) 4mg/kg neferine. Following DM induction: Group 2 (sham) received daily IP 0.25ml/kg 0.9% normal saline; Group 4 received single IP 0.01mL (2.5mg/kg) bevacizumab, followed by daily IP 0.25mL/kg 0.9% normal saline; and Group 5 received daily IP 4mg/kg neferine. Total antioxidant capacity (TAC) and total oxidative stress (TOS) levels in serum and ocular tissue homogenates were evaluated using ELISA. TUNEL method was used for determining apoptosis and immuno-histochemical staining for PCNA and VEGF immunoreactivities. Group 5 had significantly higher TAC and lower TOS in serum and ocular tissue homogenates than Group 4 (p < 0.05). Despite significantly lower VEGF levels and apoptosis (p < 0.05), there was no significant change in PCNA immunoreactivity in Group 5 (p > 0.05). DM was associated with lower TAC, higher TOS and apoptotic cells, as well as VEGF and PCNA immunoreactivities in the retina. Neferine altered parameters other than PCNA in the opposite direction, demonstrating reductive effects on DM.

Regenerative capacity of bone marrow stem cells on aged albino rat’s parotid excretory duct

ObjectiveTo appraise structural features of parotid excretory duct during senility and probable effect of bone marrow-mesenchymal stem cells (BM-MSCs). DesignA total of 14 healthy male albino rats were used. Seven adult rats (24–34-week-old) represented the control group (Group I). Seven senile rats (72–80-week-old) were utilized in which the left parotid gland served as “Old” (Group II) and were injected by 0.2 ml phosphate buffered saline; the right side represented “Old treated” (Group III) and got local injection of 1–1.5 million allogeneic BM-MSCs. One month later, glands were dissected and assessed structurally, ultra-structurally and statistically. ResultHistologically, Group I showed normal duct histology. In Group II duct lining lost its pseudostratification which was recovered in Group III. PCNA immunolocalization showed moderate reactivity in Group I, negative to mild reaction in Group II, and strong reaction in some of Group III cells. Ultra-structural features of Group I were ordinary in which basal cell had a large flat nucleus, and dark and light cells showed electron-dense cytoplasm and electron-lucent cytoplasm respectively. Tuft cell displayed long microvilli. Mucous droplets filled goblet cell. Group II revealed an apparent reduction in cells size, organelles and absence of tuft cell. In Group III all cell types were detected and they recovered their organelles, cell and nucleus shape. The highest mean area% of PCNA immunoreactivity was in Group I followed by Group III then Group II. ConclusionsAging has a deteriorating effect on structure and ultra-structure of parotid gland excretory duct that could be amended by BM-MSCs.

Zearalenone Affect the Intestinal Villi Associated with the Distribution and the Expression of Ghrelin and Proliferating Cell Nuclear Antigen in Weaned Gilts.

This study explored and investigated how zearalenone (ZEA) affects the morphology of small intestine and the distribution and expression of ghrelin and proliferating cell nuclear antigen (PCNA) in the small intestine of weaned gilts. A total of 20 weaned gilts (42-day-old, D × L × Y, weighing 12.84 ± 0.26 kg) were divided into the control and ZEA groups (ZEA at 1.04 mg/kg in diet) in a 35-d study. Histological observations of the small intestines revealed that villus injuries of the duodenum, jejunum and ileum, such as atrophy, retardation and branching dysfunction, were observed in the ZEA treatment. The villi branch of the ileum in the ZEA group was obviously decreased compared to that of the ileum, jejunum and duodenum, and the number of lymphoid nodules of the ileum was increased. Additionally, the effect of ZEA (1.04 mg/kg) was decreased by the immunoreactivity and distribution of ghrelin and PCNA in the duodenal and jejunal mucosal epithelial cells. Interestingly, ZEA increased the immunoreactivity of ghrelin in the ileal mucosal epithelial cells and decreased the immunoreactivity expression of PCNA in the gland epithelium of the small intestine. In conclusion, ZEA (1.04 mg/kg) had adverse effects on the development and the absorptive capacity of the villi of the intestines; yet, the small intestine could resist or ameliorate the adverse effects of ZEA by changing the autocrine of ghrelin in intestinal epithelial cells.

Comparison of immunohistochemical analysis on sinus augmentation using demineralized tooth graft and bovine bone.

ObjectivesThe purpose of this animal research was to compare bone regeneration in augmented rabbit maxillary sinuses treated with demineralized particulate human-tooth graft and anorganic bovine bone by immunohistochemical analysis.Materials and MethodsPiezoelectric bilateral sinus augmentation was performed in eight adult rabbits. In the control group, anorganic bovine was grafted in the maxillary sinus following elevation of the sinus membrane. In the experimental group, demineralized human particulate tooth bone was grafted in the sinus. Bone regeneration in augmented sinuses was evaluated by immunohistochemical analysis using various markers of osteoprogenitor cells.ResultsThe number of bromodeoxyuridine-labeled cells was significantly higher in the experimental group than in the control group at eight weeks. The immunoreactivity of proliferating-cell nuclear antigen was increased slightly in the experimental group relative to the control group at eight weeks. Other bone markers were expressed equally in the two groups.ConclusionIn the rabbit maxillary sinus, higher osteoinduction was correlated with demineralized human particulate tooth bone grafting than with anorganic bovine grafting.

Impact of Vitamin B17 Against Growth of Colitis Bearing Mice Induced Variations in Colon Structure, AFP, CEA and PCNA Immunoreactivity

Impact of Vitamin B17 Against Growth of Colitis Bearing Mice Induced Variations in Colon Structure, AFP, CEA and PCNA Immunoreactivity

The potential gonadoprotective effects of grape seed extract against the histopathological alterations elicited in an animal model of cadmium-induced testicular toxicity.

Grape seed extract (GSE) is a powerful antioxidant containing high levels of bioflavonoids, vitamin C and vitamin E. The aim of the work is to study the possible protective and ameliorative effects of grape seed extract in an animal model of cadmium (Cd)-induced testicular toxicity in rats. A thirty-day oral gavage study in adult male albino rats was performed using 32 animals, randomly divided into four equal groups; negative control, Cd (5 mg/k/day), GSE (100 mg/k/day), and Cd + GSE. Testicular weights were measured. Haematoxylin and eosin (H&E) staining and proliferating nuclear cell antigen (PCNA) immunohistochemistry, as a marker for proliferation were done. Morphometric parameters were assessed and subjected to statistical analysis. The H&E results showed atrophy and distortion of the seminiferous tubules (STs) with sloughing of the spermatogenic epithelium in cadmium group. The interstitial spaces were widened and showed oedema and mononuclear cell infiltrations. No remarkable changes were observed in the GSE-only group when compared to the control group. In Cd + GSE group, maintaining of the STs and their lining cells was evident. The immunohistochemical results showed marked positive PCNA immunoreactivity in both control and GSE groups, while negative immunoreaction was noticed in Cd group. Limited positive PCNA immunoreactivity was ameliorated in Cd + GSE group. Grape seed extract protected against cadmium-induced testicular toxicity in rats, reducing induced histopathological changes, and maintaining testicular histoarchitecture.

Simple, once-off mapping of various, recurrent immunostaining patterns of proliferating cell nuclear antigen in spermatogonia at the immature pole of the testis of adult wild-caught blue shark, Prionace glauca: Correlations with changes in testicular status.

This study was a single time-point mapping of various immunostaining patterns revealed with the proliferating cell nuclear antigen (PCNA) PC10 antibody in spermatogonia at the immature pole of the testis of the Blue shark (Prionace glauca). Scattered in the stroma of the germinal ridge that demarcates the immature pole's outer boundary were nests of variously immunoreactive A-spermatogonia, each flanked by a fusiform cell. Spermatocysts were assembled from niche-derived stromal cells, displaced A-progenitors, and their progeny, which showed one of two main immunostaining patterns (i.e., an uneven light brown/globular and homogeneous dark [hod] brown appearance). The testes of wild-caught Prionace showed two conditions, namely, extensive multinucleate cell death (MNC) near the mitosis-meiosis transition or an early recovery phase from the latter showing vacuolated areas. Both the proportion of cysts with immature Bhod -spermatogonia and the frequency of mitotic figures in such cysts in the early recovery testis condition were significantly higher than the comparable parameters in MNC testis condition. Moreover, the post-MNC recovery phase revealed a decrease in the proportion of immature cysts with uneven light brown/globular-like spermatogonia. The protracted spread of a cell cycle signal in an anatomically discrete, syncytially connected spermatogonial clone manifests as different PCNA immunoreactivities.