The possible ameliorative role of Lycopene on Tributyltin induced thyroid damage in adult male albino rats (histological, immunohistochemical and biochemical study).

Tributyltin is used in industrial applications. This current research aimed to study the effect of Tributyltin on the thyroid gland structure and function of adult male albino rats and the protective effect of Lycopene. Twenty-one male adult albino rats were classified into three groups: Control, treated that received Tributyltin, and protective that received Lycopene with Tributyltin. At the end of the experiment, blood samples were collected and T4, T3, and (TSH) were measured. Tissue superoxide dismutase (SOD) and malondialdehyde (MDA) were estimated. Thyroid gland specimens were processed for histological and immunohistochemical examination. Then morphometric and statistical analyses were done. The treated group showed affection in thyroid function and histological structure as vacuolated colloid and cytoplasm and dark nuclei. Ultrastructurally, follicular cells showed irregular shrunken nuclei, atrophied apical microvilli, vacuoles, multiple lysosomal granules, mitochondria with destructed cristae, and extensively dilated rough endoplasmic reticulum. There was increase in Caspase-3 immunoexpression and decrease in Beclin-1 immunoexpression. The thyroid structure and biochemical markers improved after Lycopene administration. The thyroid gland damage caused by Tributyltin is ameliorated by Lycopene.

A comparative study between the possible protective role of melatonin versus its combination with adipose derived-mesenchymal stem cells on experimentally induced diabetic retinopathy in adult male albino rats (Histological and immunohistochemical study).

Diabetes mellitus is a metabolic disorder that can cause numerous ocular issues as well as long-term effects. In our study, we evaluate the effect of melatonin on the diabetic retinal alterations in male albino rats to the effect of melatonin combined with stem cells. 50 adult male rats were equally divided into four groups control, diabetic, melatonin, and melatonin plus stem cells. STZ, 65 mg/kg in phosphate buffered was administered intraperitoneally as a bolus to diabetic group of rats. After inducing diabetes, melatonin (10 mg/kg b.wt./day) was administered orally to the melatonin group for 8 weeks. The stem cell and melatonin group got the same dosage of melatonin as the prior group. They received an intravenous injection of (3?×?106 cell) adipose-derived MSC suspended in phosphate-buffered saline at same time of melatonin ingestion. Animals from all groups had their fundics examined. Following the injection of stem cells, samples of rat retina were collected for light and electron microscopy analyses. H&E and immunohistochemically stained sections revealed a slight improvement in group (III). At the same time, group (IV) results were comparable to those of the control group, which was supported by the findings of an electron microscope. Neovascularization was visible on fundus examination in group (II), whereas it was less noticeable in group (III) and group IV. Melatonin mildly improved the histological structure of the retina in diabetic rats, and when it was combined with adipose-derived MSC, it considerably improved the diabetic alterations.

Infliximab abrogates adenine-induced chronic kidney disease via modulation of the MAPK/JNK/ASK signaling pathway in rats.

Chronic kidney disease (CKD) is a prominent cause of death worldwide. Infliximab is one of the anti-TNF-α; herein, we studied the effect of infliximab on adenine-induced CKD. To inspect the role of infliximab, either ameliorative or curative, on CDK induced with adenine. Thirty Wistar albino rats were separated into five groups of 6 rats' each: rats of group Ι were kept as control given saline, rats of group II were treated with infliximab (5 mg/kg, i.p.) for 5 weeks, rats of group ΙΙΙ (the diseased group) had an adenine containing diet (0.25% W/W in feed) for 5 weeks, rats of group ΙV (the ameliorative group) had an adenine-containing diet and infliximab (5 mg/kg, i.p.) for 5 weeks simultaneously, and rats of group V (the curative group) had adenine containing diet then a single dose of infliximab (5 mg/kg, i.p.) was given in the 6th week. Infliximab treatment revealed a decrease in the plasma levels of urea, creatinine, NGAL, and MDA with a substantial increase in TAC. Also, inflammatory mediators such as IL-6 and NF-κB were significantly decreased with the down-regulation of the ASK1/MAPK/JNK pathway. Caspase 3 was downregulated. Also, infliximab treatment exhibited improvement in the histological and immunohistochemical kidney changes. Through its involvement in reducing oxidative stress, inflammation, and apoptosis, infliximab has an ameliorative and curative effect on CKD induced with adenine.