Levels Of Histopathological Changes Research Articles

Effectiveness of Histopathological Changes of Induced Thin Layer Endometrium by Pentoxifylline and Pentoxifylline-Loaded Poly Lactic-co-Glycolic Acid on Female Rats.

Pentoxifylline (PTXF) is a vasoactive agent that plays a significant role in the treatment of thin-layer endometrium cases. The PTXF, also identified as oxpentifylline, is a member of xanthine derivatives and a competitive nonselective phosphodiesterase inhibitor leading to the elevation of intracellular cAMP, inhibition of tumor necrosis factor and leukotriene synthesis, activation of protein kinase A, and reduction of inflammation and innate immunity. Moreover, it is used as an agent to relieve muscle pain in people with peripheral artery disease (vascular irregularities). It is also an acceptable choice for the treatment of radiation-induced fibrosis. Therefore, the present study aimed to determine the advantageous impact of PTXF and PTXF-loaded poly lactic-co-glycolic acid (PLGA) on female rats after being exposed to ethanol to create a thin layer of the endometrium. For this purpose, 50 female rats were selected and divided into five groups (G1: negative normal control, G2: positive control, G3: PLGA only, G4: preference PTXF, and G5: PLGA-PTXF groups) for a 20-day treatment period. In this study, the histopathological section revealed a perfect improvement in the tissues of the uterine horn of female rats that induced endometria and were treated with PLGA-PTXF. In this group of rats, clear healing was achieved and there was an increase in the thickness of endometrium and myometrium, compared to the ordinary PTXF-treated group which had the lowest recovery characteristics. However, the positive control group underwent a significant decrease in terms of endometrium and myometrium thickness as well as vascular and glandular density. This study showed that the PTXF-loaded PLGA had the capacity to heal the thin layer of the endometrium by improving the levels of histopathological changes, especially regarding the thickness of the endometrium and myometrium more than the ordinary PTXF.

Protective effect of Saussurea involucrata polysaccharide against skin dryness induced by ultraviolet radiation.

Background: Exposure to ultraviolet B (UVB) radiation can damage the epidermis barrier function and eventually result in skin dryness. At present, little work is being devoted to skin dryness. Searching for active ingredients that can protect the skin against UVB-induced dryness will have scientific significance. Methods: Saussurea involucrata polysaccharide (SIP) has been shown to have significant antioxidant and anti-photodamage effects on the skin following UVB irradiation. To evaluate the effect of SIP on UVB-induced skin dryness ex vivo, SIP-containing hydrogel was applied in a mouse model following exposure to UVB and the levels of histopathological changes, DNA damage, inflammation, keratinocyte differentiation, lipid content were then evaluated. The underlying mechanisms of SIP to protect the cells against UVB induced-dryness were determined in HaCaT cells. Results: SIP was found to lower UVB-induced oxidative stress and DNA damage while increasing keratinocyte differentiation and lipid production. Western blot analysis of UVB-irradiated skin tissue revealed a significant increase in peroxisome proliferator-activated receptor-α (PPAR-α) levels, indicating that the underlying mechanism may be related to PPAR-α signaling pathway activation. Conclusions: By activating the PPAR-α pathway, SIP could alleviate UVB-induced oxidative stress and inhibit the inflammatory response, regulate proliferation and differentiation of keratinocytes, and mitigate lipid synthesis disorder. These findings could provide candidate active ingredients with relatively clear mechanistic actions for the development of skin sunscreen moisturizers.

Keratinocyte Growth Factor 2 Ameliorates UVB-Induced Skin Damage via Activating the AhR/Nrf2 Signaling Pathway.

Objective: Exposure to ultraviolet B (UVB) can cause skin damage through oxidative stress, DNA damage, and apoptosis. Keratinocyte growth factor (KGF) has been shown to reduce the content of intracellular reactive oxygen species (ROS) following UVB exposure, a role that is crucial for the efficient photoprotection of skin. The present study evaluated the photoprotective effect of KGF-2 on UVB-induced skin damage and explored its potential molecular mechanism. Methods: To evaluate the effect of KGF-2 on UVB-induced damage ex vivo, a human epidermal full-thickness skin equivalent was pretreated without or with KGF-2 and then exposed to UVB and the levels of histopathological changes, DNA damage, inflammation, and apoptosis were then evaluated. The ability of KGF-2 to protect the cells against UVB-inflicted damage and its effect on ROS production, apoptosis, and mitochondrial dysfunction were determined in HaCaT cells. Results: Pretreatment of the epidermis with KGF-2 ameliorated the extent of photodamage. At the cellular level, KGF-2 could attenuate ROS production, apoptosis, DNA damage, and mitochondrial dysfunction caused by UVB exposure. KGF-2 could also activate the aryl hydrocarbon receptor (AhR) to trigger the Nrf2 signaling pathway. Conclusion: Taken together, our findings suggested that KGF-2 could ameliorate UVB-induced skin damage through inhibiting apoptosis, reducing oxidative stress, and preventing DNA damage and mitochondrial dysfunction via regulating AhR/Nrf2 signaling pathway.

Macrophage Activity and Histopathological Differences of Lung Tissue on Sequential Co-infections of Heligmosomoides Polygyrus Nematode on Mycobacterium Tuberculosis Infection

Background: Tuberculosis is a chronic infection caused by Mycobacterium tuberculosis, a facultative intracellular parasite, that can be eliminated by cellular immunity played by macrophages. It has become a debate whether the co-infection of nematodes will affect the immune response of macrophages towards mycobacterium infection. Objective: To reveal macrophage activity and histopathological difference of lung tissue in sequential coinfection of Heligmosomoides Polygyrus towards Mycobacterium tuberculosis infection. Method: This study used 49 mice divided into 7 treatment groups with Mycobacterium tuberculose infection by inhalation and Heligmosomoides polygyrus orally within 8 and 16 weeks, and observed by immunohistochemical staining. Result: Infection for 8 weeks showed polarization of macrophages towards M1 macrophage, whereas in 16 weeks, the macrophage polarization more towards M2 macrophages, supported by histopathological changes of lung tissue: peribronchiolitis, perivaskulitis, alveolitis, and granuloma formation with counts of acid-resistant germs +3. There was a difference of expression of arginase1 to each group (p <0.001) and there was a difference of T CD4+ Th1 lymphocyte (p <0.001). Conclusion: There is a difference in macrophage activity in lung tissue; however, it does not cause different levels of histopathological changes in lung tissue and does not affect the immune response to Mycobacterium tuberculosis infection.

Gentamicin Nephrotoxicity in Animal Model: Study of Kidney Histopathology and Physiological Functions

The purpose of this study was to analyze abnormal changes in kidney histology and physiology in acute kidney injury animal models with multiple doses of gentamicin. Induction of experimental animals was carried out on 20 rats (Rattus norvegicus) Wistar strain which were divided into 4 groups, group I was a negative control group, groups II, III and IV are gentamicin-induced groups at doses of 30 mg/kg, 40 mg/kg, and 50 mg/kg, respectively. Kidney histopathology were stained with Hematoxylin Eosin (HE), while analysis of serum BUN and creatinine by spectrophotometric method. Data analysis for kidney histopathology was descriptively while for BUN and Creatinine were statistically tested with one way ANOVA. The results of this study showed there was a kidney damage in all gentamicin-induced groups, which is necrosis in the contortus tubule and the Bowman’s capsule compared to the negative control group. The group of rats with the higher doses of gentamicin showed a more severe level of histopathological changes, however, BUN and creatinine levels were not significantly different (p> 0.05). This study concludes that gentamicin induction could cause kidney histopathological changes but not kidney physiology.

Histological, morphometric, protein and gene expression analyses of rat retinas with ischaemia-reperfusion injury model treated with sildenafil citrate.

The aim of this study was to better understand the role of apoptosis in a retinal ischaemia-reperfusion injury model and to determine whether sildenafil citrate treatment can prevent retinal cell apoptosis. Thirty-six rats were divided into a control group (n=6) and two experimentally induced ischaemia-reperfusion groups (7 and 21days; n=15 per group). The induced ischaemia-reperfusion groups were treated with sildenafil for 7 and 21days (n=10 per group), and 10 animals were treated with a placebo for the same period (n=5 per group). Paracentesis of the anterior chamber was performed with a 30-G needle attached to a saline solution (0.9%) bag positioned at a height of 150cm above the eye for 60min. Intraocular pressure was measured by rebound tonometer (TonoVet® ). The eyes were analysed by histology and morphometry, and by immunohistochemistry and qRT-PCR for expression of Caspase-7, Caspase-6, Caspase-9, Tnf-r2, Fas-l, Bcl-2 and Bax. Sildenafil-treated animals showed lower levels of histopathological changes (inflammatory, cellular and tissue) than their placebo-treated counterparts at both 7 and 21days. The retinal ganglion cell layer (RGC) was preserved in the sildenafil groups (SG), with a cell count closer to control than in the placebo groups (PG). Caspase-7 expression was significantly higher in both treated groups at 7days compared to controls. Gene expression levels in both treatment groups differed from the controls, but in SG Bax and Caspase-6 expression levels were similar to control animals. These results suggest that the main mechanism of retinal cell death in this model is apoptosis, as there is an increase in pro-apoptotic factors and decrease in the anti-apoptotic ones. Also, sildenafil seems to protect the retinal ganglion cell layer from apoptosis. Cell survival was evident in the histological and morphometric analyses, and sildenafil treatment had a protective effect in the apoptosis pathways, with gene expression levels in SG similar to the controls.

Melatonin protects against burn-induced hepatic oxidative injury by inducing HO-1 via the Nrf2 pathway

Melatonin exerts beneficial effects on early liver injury by modulating hepatic oxidative stress. In order to understand the protective effect of melatonin against burn-induced hepatic injury we investigated the expression of 4-hydroxynonenal (4-HNE), a main product of lipid peroxidation and mediator of oxidative injury, the inducible heme-oxygenase-1 (HO-1), an antioxidant enzyme, and the anti-oxidative stress regulator erythroid 2-related factor 2 (Nrf2) in a burn rat model. Expression and localisation of HO-1, 4-HNE and Nrf2 in liver were investigated using light immunochemistry. Thermal skin injury caused a significant elevation in hepatic 4-HNE and degenerative liver changes. Concurrently, there was increased expression of HO-1, a rate-limiting enzyme for haem degradation and an oxidative stress marker in sinusoidal endothelial cells (SECs) and hepatocytes without changes in Nrf2 expression in the liver. Melatonin (20 mg/kg b.w.) augmented the increase in HO-1 expression, upregulated Nrf2 expression and also led to decreased 4-HNE levels and reduced levels of histopathological changes in rat liver. In conclusion, our results suggest that melatonin ameliorates burn-induced liver injury through the inhibition of oxidative stress, upregulation of the antioxidant enzyme HO-1 and activation of the antioxidant Nrf2 pathway. Stimulation of cellular protective mechanisms by activating the antioxidant stress response through Nrf2 is a new mechanism for protection against liver damage in burns.

Use of histopathology and elemental accumulation in different organs of two benthophagous fish species as indicators of river pollution

The bottom feeding fish species have a good potential to be used for assessments of pollution, as they are under pressure from pollutants from both water and sediments. In this study, the level of similarity of histopathological responses to pollution in gills and liver between barbel (Barbus barbus) and sterlet (Acipenser ruthenus) from the Danube River was assessed, and compared with elemental concentrations in their gills, liver, and muscle. Results indicate that the detected metal concentrations were likely cause of different tissue responses in gills and liver of the two investigated fish species. Statistical analysis indicated a clear differentiation of the two species based on elemental concentrations and the level of histopathological changes in gills and liver. Metal concentrations exceeded maximum acceptable concentrations in a number of analyzed specimens, which indicates the importance of this type of monitoring. Results indicate that barbel is a better indicator for specific, rather narrow sites, whereas sterlet is a better indicator of larger (longer) water current segments. Obtained information could be of importance for both scientists and fishery and water management authorities working on the development of water monitoring programs.

Histopathological indicators: a useful fish health monitoring tool in common carp (Cyprinus carpio Linnaeus, 1758) culture

Abstract In order to evaluate the relationship between water quality in ponds and indices of histopathological changes occurring in the vital organs of the common carp (Cyprinus carpio L., 1758), two six-month field experiments were carried out using two different water supplies: from the nearby stream and a tube well. The fish were fed supplemental feed: raw cereals, pelleted and extruded compound feed. Histopathological analysis, alteration frequencies, and semi-quantitative scoring of the changes were used to assess the health status of the fish. Ponds supplied by stream water were characterized by higher water hardness, dissolved oxygen and pH values, while those supplied by the tube well had higher electroconductivity, total ammonium and orthophosphates content. Fish survival rate and habitat suitability index were lower in ponds supplied by stream water, while the weight gain did not differ between the two water supplies. The use of stream water resulted in a higher level of histopathological changes in gills and liver. Among the water quality parameters, pH level had the strongest influence on fish. Differences in water supply produced greater influence on the level of histopathological changes than the type of feed applied. Gills were the most sensitive organ, while the kidney was the least responsive.

Lack of detectable enhanced pulmonary histopathology in cotton rats immunized with purified F glycoprotein of respiratory syncytial virus (RSV) when challenged at 3–6 months after immunization

The cotton rat model has been used to evaluate the potential for immunogens to induce respiratory syncytial virus (RSV)-enhanced pulmonary histopathology. A recent study evaluated purified F protein in this model when animals were challenged intranasally with RSV 3 or 6 months after immunization. The authors concluded that the purified F protein was associated with the same level of histopathological changes as observed with the positive control, a formalin-inactivated RSV immunogen. Three pathologists have independently evaluated the lung sections from the animals of this study and the results are reported in this article. In contrast to the previously published data, we have found that F protein was associated with a substantially milder and qualitatively different response to that observed with the formalin-inactivated RSV vaccine. We concluded that the minimal histological changes observed and lack of clinical disease make it very difficult to assess the issue of enhanced pulmonary RSV disease with the cotton rat model.

A critical evaluation of the acute systemic toxicity test for dental alloys using histopathologic criteria

The A.D.A. acute systemic test for type II, class 11 materials defines compliance on the basis of fewer than 50% mortality at 2 weeks. Histopathologic criteria were developed from pilot study data to evaluate the effects of these materials. In this double blind study, the frequency of histopathological changes in lung, liver, small intestine, and kidney were rated at 2 and 5 weeks, for six dental crown and bridge alloys ranging from 44% to 97% (Au, Pt, and Pd). Two positive 360 mg/kg and 1 g/kg of cadmium and two negative, a blank capsule and untreated control groups were used. There was significant difference (chi square test, X2 = 0.95) between the positive and negative controls at 2 and 5 weeks. The lung, liver, kidney showed the highest level of histopathological changes. Significant changes occurred in the four tissues for all alloys at two and five weeks. At five weeks, alloys with a lower noble metal content (44-62%, Au, Pd, and Pt) elicited significant chronic changes, while higher noble metal content (78-97%) showed healing and no significant difference from the negative controls. Applying histopathologic criteria and statistical parameters independent examiners can examine experimental animals and arrive at conclusive and reproducible results.