Lycopene attenuates bisphenol A-induced lung injury in adult albino rats: a histological and biochemical study.

Bisphenol A (BPA) leads to ROS production that considered the core of different inflammatory and chronic obstructive pulmonary diseases. As a natural antioxidant, lycopene plays a significant role in the prevention of many chronic diseases. This study aimed to investigate the possible protective role of lycopene against BPA-induced lung alterations using morphometric, histological, immunohistochemical and biochemical methods. Forty rats aged 3 months were divided into four groups (n=10): control group, lycopene group comprising rats that received lycopene by gavage (10 mg/kg /day) for 30 days, BPA group comprising rats that received BPA by gavage (50 mg/kg/day) for 30 days and lycopene + BPA group. On the 30th day, blood and lung tissue samples were collected for biochemical, histological and immunohistochemical studies. Morphometrical and statistical analyses were performed. The BPA group revealed significantly elevated IL-1B, IL-6, MDA and NO, and it showed significantly reduced IL-10, SOD, CAT and GSH when compared to the control and lycopene + BPA groups. Upon histopathological and immunohistochemical examination, lycopene supplementation improved the BPA-induced alveolar collapse, lymphocytic infiltration, extravasated RBCs and fibrosis. The lycopene + BPA group showed significantly reduced mean percentage of 8-OHdG immunopositive and mean area percentages of Bax and caspase 3 immunopositive cells and significantly reduced mean area percentage of Bcl2 immunopositive cells as compared with the BPA group. Lycopene is a protective agent against BPA-induced lung injury because of its anti-apoptotic, anti-inflammatory and antioxidant effects, as confirmed by biochemical and histological studies.

The counteracting effects of (-)-Epigallocatechin-3-Gallate on the immobilization stress-induced adverse reactions in rat pancreas.

Many studies suggest that Epigallocatechin-3-Gallate (EGCG) has many protective effects. But little is known about its protective effects against chronic restraint stress-induced damage in rats. The aim was to demonstrate the potential protective effects of EGCG against harmful pancreatic damage to the immobilization stress in the rat model. Forty rats, 2 months old, were divided into four groups (n = 10): control group; EGCG group, rats received EGCG by gavage (100 mg/kg /day) for 30 days; stressed group, rats exposed to immobilization stress; and stressed with EGCG group, rats exposed to immobilization stress and received EGCG for 30 days. Glycemic status parameters, corticosterone, and inflammatory markers were investigated on the first day, 15th day, and the 30th day of the experiment. Pancreatic oxidative stress markers and cytokines were evaluated. Histological, immunohistological, and statistical studies were performed. On the 15th day, fasting blood glucose (FBG), fasting plasma insulin (FPI), homeostatic model assessment for insulin resistance (HOMA-IR), and fasting plasma corticosterone were significantly higher in the stressed group when compared with first and 30th day in the same group as well as when compared with control and stressed with EGCG groups. The stressed group revealed significantly higher pancreatic IL-1ß, IL-6, TNF-α, MDA, and NO, serum amylase and serum lipase, and significantly lower GSH, SOD, and CAT when compared to control and stressed with EGCG groups. EGCG treatment attenuated the pancreatic stress-induced cellular degeneration, leucocytic infiltration, and cytoplasmic vacuolations; significantly decreased area percentage of collagen fibers; and significantly increased mean area percentage of insulin immunopositive cell as compared with stressed group. EGCG is a protective agent against immobilization stress because of its anti-diabetic, anti-inflammatory, and and anti-oxidative stress properties, as confirmed by biochemical and histological alterations.

Neuroprotective role of curcumin on the hippocampus against the structural and serological alterations of streptozotocin-induced diabetes in Sprague Dawely rats.

OBJECTIVES: Diabetes mellitus causes impaired memory and cognitive functions. The hippocampus plays a key role in memory and learning. Curcumin attenuates diabetic nephropathy in vivo. Curcumin has shown a neurogenic effect and cognition-enhancing potential in aged rats. The aim of this study is to evaluate the possible protective role of curcumin on the histological and serological changes of the hippocampus in diabetic rats. MATERIALS AND METHODS: Forty albino rats were divided into four groups, ten rats each. Group 1 control rats, group 2 rats received curcumin orally (200 mg/kg/day for six weeks), group 3 rats were injected intraperitoneally with streptozotocin (STZ) (100 mg/kg, single dose), group 4 received a single injection of STZ and received curcumin orally for six weeks. Paraffin sections of hippocampus were prepared and stained with hematoxylin and eosin stain, and immnunohistochemical staining for GFAP and caspase-3. Morphometrical and statistical analyses were performed. Glycemic status and parameters of oxidative stress was measured. RESULTS: Examination of hippocampus of diabetic rats showed disorganization of small pyramidal cells in CA1, many cellular losses in the pyramidal cells of CA3, many degenerated granule cells in the dentate gyrus. GFAP positive astrocyte and caspase-3 positive neuron counts were significantly increased. There were significant serum glucose elevation and significant lowered levels of oxidative stress parameters as compared to control rats. Curcumin administration improved the structural and serological alterations of the hippocampus with significant reduction in serum glucose level. CONCLUSION: Curcumin ameliorates the deterious effect of diabetes on the hippocampus through its antioxidant, antiapoptotic and anti-inflammatory efficacies.