Histological study of the effect of granulocyte colony-stimulating factor on experimentally induced corneal burn in adult male albino rats.

Chemical injuries to the eye represent one of the true ophthalmic emergencies that require immediate and intensive intervention to minimize severe complications and visual loss. Granulocyte colony-stimulating factor (G-CSF) is a potent hematopoietic cytokine that influences the proliferation, survival, maturation, and the functional activation of granulocytes. The present work was performed to evaluate the histological effect of G-CSF in treating rat corneal alkali burn model. Thirty adult male albino rats were divided equally into three main groups: Group I was served as a control group, and in Group II and III, their corneas of the right eyes were injured by applying a piece of filter paper soaked in 1M NaOH. Group II (alkali burn-induced group) was left without any treatment, while Group III (G-CSF-treated group) was injected subcutaneously by 100 µg/kg of G-CSF for 5 consecutive days. All animals were sacrificed after 3 weeks. Cornea specimens were processed for histological and immunohistochemical staining for P63 followed by morphometry. Microscopic examination of Group II revealed marked alterations in the corneal epithelium, inflammatory cellular infiltration, and neovascularization. Treatment with G-CSF showed great improvement of the corneal structure, disappearance of the neovascularization and the inflammatory cells, and decreased p63 reaction of the basal layers.

An industrial procedure for the intestinal permeability enhancement of acyclovir: in-vitro and histological evidence.

Acyclovir, an antiviral drug, has low bioavailability due to its low permeability. Consequently, high drug doses and frequent administration are required. This study investigates the use of span 60, at different concentrations, as a granulating agent to enhance drug permeability using an industrial procedure on a pilot scale. The micromeritics, drug content, drug crystallinity, drug partition coefficient, and drug release of the produced formulations were examined. The findings revealed an enhanced drug partition coefficient, suggesting drug entrapment in the polar portion of span 60. The drug release profiles exhibited rapid and complete drug release. The improvement of the drug permeability was evaluated using a modified non-everted sac technique. Notably, drug permeability through the rabbit intestine significantly improved, as evidenced by various calculated permeation parameters, providing insights into the drug absorption mechanism. The widening of the paracellular pathway was observed through histological examination of the rabbit intestinal segment, which aligns with the drug absorption mechanism. The utilization of a paracellular pathway enhancer as a granulating agent holds promise as a strategy to enhance the oral bioavailability of class III drugs. Overall, this study presents a novel drug delivery approach to enhance drug permeation and bioavailability, with potential implications for other medications.

Fisetin ameliorates oxidative glutamate testicular toxicity in rats via central and peripheral mechanisms involving SIRT1 activation.

OBJECTIVES: This study aimed to evaluate the potential mitigating effect of fisetin on monosodium glutamate (MSG)-induced testicular toxicity and investigate the possible involvement of silent mating type information regulation 2 homolog 1 (SIRT1) in this effect. METHODS: Forty male rats were divided into normal control, fisetin-treated, MSG-treated, and fisetin + MSG-treated groups. Testosterone, GnRH, FSH, and LH were measured in plasma, as well as SIRT1 and phosphorylated AMP-activated protein kinase (pAMPK) levels in testicular tissues using ELISA. Hydrogen peroxide (H2O2), nitric oxide (NO), and reduced glutathione (GSH) were measured colorimetrically, while Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) expression was relatively quantified using RT-PCR in testicular tissues. RESULTS: After 30 days, fisetin could ameliorate MSG-induced testicular toxicity by acting centrally on the hypothalamic-pituitary-gonadal axis, increasing plasma levels of GnRH, FSH, LH, and testosterone. Peripheral actions of fisetin on the testis were indicated as it increased testicular SIRT1 and pAMPK. Furthermore, it antagonized glutamate-induced oxidative stress by significantly lowering H2O2, NO, and relative NOX4 expression while significantly increasing reduced GSH levels. It also improved the architecture of the seminiferous tubules, reduced sperm abnormality, and increased sperm count. DISCUSSION: Fisetin ameliorates MSG-induced testicular toxicity via central and peripheral mechanisms making it a promising therapeutic target for male infertility.