Silymarin administration protects against cisplatin-induced nephrotoxicity in adult male albino rats. [histological and immunohistochemical study]

Cisplatin is one of the most commonly used chemotherapeutics for cancer treatment, but its use is limited because of its nephrotoxicity Several evidences suggested that cisplatin-induced nephrotoxicity is partially mediated by reactive oxygen species. The purpose of the present study is to investigate whether silymarin administration as an antioxidant before cisplatin could afford protection against cisplatin-induced nephrotoxicity. This study was performed on 30 adult male albino rats that were divided into 5 groups. Group 1: served as control group. Animals of other groups received a single intraperitoneal [IP] injection of the following treatments: Group II received 0.1ml of normal saline+1% w/v methylcellulose, Group III received silymarin [50 mg/kg BW], Group IV: Received cisplatin [7.5 mg/kg BW] and Group V: Received silymarin 6 h before cisplatin injection. Kidneys were excised 5 days after the end of the experiment biopsies were processed for light microscopic studies. Immunohistoehemical expression of Bak protein was investigated. Renal cortex of group IV showed extensive renal tubularnecrosis, intratubular casts, desquamated renal tubular cells, cytoplasmic degeneration and mononuclear cellular infiltration. The cells of proximal convoluted tubules [PCT] were severely affected. Also, there was a decrease in the PAS +ve material at brush borders of the PCT and a positive cytoplasmic reaction of Bak protein in renal tubular cells. There were statistical significant differences regarding these changes when compared to the other groups. In group V, the renal cortex of examined animals appeared similar to control group. Silymarin pretreatment prevented the histopathological changes caused by cisplatin. Therefore, silymarin can be used as an effective protecting agent against cisplatin-induced nephrotoxicity

protective role of alpha-Lipoic acid against doxorubicin-induced cardiotoxicity in male albino rats [a light and transmission electron microscopy study]

Doxorubicin [DOX] is an important anti-neoplastic agent. Cardiotoxicity, which mediated by free radicals, is the main side effect of it, leads to induce left ventricular systolic dysfunction and congestive heart failure. The aim of the present study was to investigate the postulated preventive role of alpha-lipoic acid [LA] which is capable of neutralizing a wide variety of free radicals against doxorubicin [DOX]-induced cardiotoxicity. Twenty adult male albino rats were used in this study. They were randomized into four groups [5 rats! group]. Group I [control] received a single intraperitoneal [IP] injection of 3 ml of sterile distilled water. Group II [control LA] received a single IP injection of 3 ml of sterile distilled water and LA [100 mg/kg BW!day] orally for 7 days. Group III [Dox-injected group] received a single IP dose of Dox [1 5mg/kg BW in 3 ml of sterile distilled water]. Group IV received LA as in group II for 5 days before and 2 days after DOX injection. Animals were sacrificed 48 hours after DOX injection. Specimens from the left ventricle of the heart were processed for histological [H and E; Masson's trichrome] and ultra-structural study. Quantitative measurements [cardiomyocyte diameter and color area percentage of collagen] were done using image analyzer [Super eye-Heidi soft]. Group I and II showed no changes. Light microscopic results of group III showed damage and necrosis of cardiomycytes in addition to congestion and mononuclear cellular infiltration. The cardiomyocytic diameter and the surrounding fibrous tissue were significantly increased in this group compared to other studied groups. Ultrastructural results showed loss of cross striation and mitochondrial degeneration. These deleterious changes were significantly improved in group IV. DOX induced cardiotoxicity can be protected by using LA

Narrow-band UVB decreases epidermal thickness, mast cell density and downregulates IL-8 expression in psoriatic lesions histological and immunohistochemical study

The increased epidermal thickness and number of early activated cutaneous mast cells is a typical feature of psoriatic inflammation. Over expression of IL-8 and its receptor CXCR2 is typically observed in psoriasis lesions and is thought to contribute to keratinocyte dysfunction and to influx of T cells, neutrophils and mast cells. This study was conducted to evaluate epidermal thickness, mast cell density and IL-8 expression in psoriatic lesions before and after narrow-band ultraviolet B [NB-UVB] therapy using histological and immunohistochemical techniques. Twenty five psoriatic patients referred from Dermatology Outpatient Clinics for NB-UVB phototherapy were enrolled in this study. Patients received irradiation with NB-UVB [312 nm, Philips TL01] on the whole body. Four groups were included in this study; control group [1]: normal skin from 5 healthy volunteers], control group [2]: non-lesional control group; normal skin from psoriatic patients,Pre-NB-UVB group: twenty five psoriatic patients and Post- NB-UVB group: psoriatic patients after NB-UVB treatment. Skin biopsies were taken, fixed, processed and stained to assess general skin structure: and epidermal thickness, mast cell density and IL-8 expression by using histological and immunohistochemical procedures. After NB-UVB therapy; there was significant improvement in PASI score and significant decrease in epidermal thickness, mast cell density and optical density of IL-8. NB-UVB therapies targeting epidermal thickness, mast cells or IL-8 should be considered in the treatment of psoriasis