The antioxidant effects of coenzyme Q10 on albino rat testicular toxicity and apoptosis triggered by bisphenol A.

Polycarbonate plastics for packaging and epoxy resins are both made with the industrial chemical bisphenol A (BPA). This investigation looked at the histological structure, antioxidant enzymes, and albino rats' testis to determine how coenzyme Q10 (CoQ10) impacts BPA toxicity. For the experiments, three sets of 18 male adult rats were created: group 1 received no therapy, group 2 acquired BPA, and group 3 got the daily BPA treatment accompanied by coenzyme Q10, 1 h apart. The experimental period ran for 14 days. The biochemical biomarkers catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA) were altered as a result of BPA exposure. The testicular histological architecture, which is made up of apoptosis, was also exaggerated. Furthermore, rats given BPA and CoQ10 treatment may experience a diminution in these negative BPA effects. These protective properties of CoQ10 may be correlated with the ability to eliminate oxidizing substances that can harm living species. The outcomes might support the hypothesis that CoQ10 prevented oxidative damage and boosted rats' stress responses when BPA was introduced. Thus, by shielding mammals from oxidative stress, CoQ10 aids in the growth and development of the animals. BPA is extremely hazardous to humans and can persist in tissues. Human reproductive functions are a worry due to human exposure to BPA, especially for occupational workers who are typically exposed to higher doses of BPA. As a result, in order to reduce the health risks, BPA usage must be minimized across a diverse range of industries, and improper plastic container handling must be prohibited. By giving CoQ10 to patients, BPA's harmful effects on reproductive structures and functions may be avoided.

The possible effects of α-tocopherol against amiodarone-treated lungs in rats: vimentin detection, lipid peroxidation assay, and histological and ultrastructural evaluations.

The purpose of this study was to learn more about the pathogenesis of amiodarone (AD) on alveoli and also the possible preventive effect of α-tocopherol (α-T) against these hazards. Rats were divided into 4 groups, one of which acted as a control, the second received α-T, the third AD, and the fourth AD and α-T for 2 weeks. Light microscopy (LM), immunohistochemistry, transmission electron microscopy (TEM), and malondialdehyde (MDA) activity were analyzed in sections of lung tissue. Alveoli of lung tissue AD examined with LM showed dilatation of alveolar spaces, aggregation of red blood cells, and narrowing of alveolar septa. When stained with vimentin (VIM), alveoli showed a positive reaction in the majority and a moderate reaction in others. In the pneumocytes of the type II, some cytoplasmic vesicles had been deflated, whereas others contained lamellar bodies, a damaged nucleus, and vesicles in their heterochromatin. In the interstitial space, collagen fibers with aggregation of red blood cells and a disrupted blood-air barrier were detected. In rat lung alveoli treated with AD and α-T, the alveolar septum thickened and the alveolar spaces expanded as estimated. The alveoli of this group had more or less intact type I and II pneumocytes and a better appearance of the blood-air barrier. In the cells of the alveolar lining, the VIM staining leads to a diffuse positive response. Finally, lung parenchyma also improved, suggesting that α-T may help minimize the effects of AD.

The ameliorative effect of kaempferol against CdCl2- mediated renal damage entails activation of Nrf2 and inhibition of NF-kB.

This study evaluated the nephroprotective effect of kaempferol against cadmium chloride (CdCl2) -induced nephropathy in rats. It also investigated if activation of Nrf2 is a common mechanism of action. Adult male rats ((150 ± 15 g) were divided into 4 groups (n = 8/each) as a control (1% DMSO, orally), control + kaempferol (200 mg/kg, orally), CdCl2 (50 mg/l in drinking water), and CdCl2 + kaempferol (200 mg/kg)-treated rats. All treatments were conducted for 8 weeks. Kaempferol significantly attenuated CdCl2-induced weight loss, reduction in kidney weights, and the injury in the glomeruli, proximal tubules, and distal tubules in the treated rats. It also significantly lowered serum levels of urea and creatinine, increased urine output and urinary creatinine levels and clearance but reduced urinary levels of albumin urinary albumin exertion (UAER), and urinary albumin/creatinine ratio (UACR) in these rats. In parallel, kaempferol downregulated renal levels of cleaved caspase-3 and Bax and unregulated those of Bcl2. In the kidney tissues of the control animals and CdCl2 rats, kaempferol significantly attenuated oxidative stress, inflammation and significantly boosted levels of manganese superoxide dismutase and glutathione. Also, and in both groups, kaempferol suppressed the nuclear levels of NF-κB p65, downregulated Keap1, and stimulated the nuclear activation and protein levels of Nrf2. In conclusion, kaempferol is a potential therapeutic drug to prevent CdCl2-induced nephropathy due to its anti-inflammatory and anti-oxidant effects mediated by suppressing NF- NF-κB p65 and transactivating Nrf2.

Salidroside inhibits insulin resistance and hepatic steatosis by downregulating miR-21 and subsequent activation of AMPK and upregulation of PPARα in the liver and muscles of high fat diet-fed rats.

This study evaluated if salidroside (SAL) alleviates high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) by downregulating miR-21. Rats (n = 8/group) were treated for 12 weeks as normal diet (control/ND), ND + agmoir negative control (NC) (150 µg/kg), ND + SAL (300 mg/kg), HFD, HFD + SAL, HFD + compound C (an AMPK inhibitor) (200 ng/kg), HFD + SAL + NXT629 (a PPAR-α antagonist) (30 mg/kg), and HFD + SAL + miR-21 agomir (150 µg/kg). SAL improved glucose and insulin tolerance and preserved livers in HFD-fed rats. In ND and HFD-fed rats, SAL reduced levels of serum and hepatic lipids and the hepatic expression of SREBP1, SREBP2, fatty acid (FA) synthase, and HMGCOAR. It also activated hepatic Nrf2 and increased hepatic/muscular activity of AMPK and levels of PPARα. All effects afforded by SAL were prevented by CC, NXT629, and miR-21 agmoir. In conclusion, activation of AMPK and upregulation of PPARα mediate the anti-steatotic effect of SAL.

Immunomodulatory effects of bee pollen on doxorubicin-induced bone marrow/spleen immunosuppression in rat.

This study investigated the immunomodulatory effects of Bee Pollen (BP) on Doxorubicin (DOX)-induced bone marrow/spleen suppression in rats. 48 Wistar rats were divided into 6 groups (n = 8/group); control, DOX (5 mg/kg), BP (100 mg/kg), BP (200 mg/kg), BP (100 mg/kg) +DOX, and BP (200 mg/kg) +DOX groups. BP was administered orally for 42 days and 5 mg/kg of DOX was injected intravenously at days 7, 14, 21, 28, 35 and 42. Hematological parameters, antioxidant enzymes and inflammatory cytokines were measured. Apoptosis-related genes were investigated using Real-Time PCR and western blot. DOX significantly decreased blood cells count, cytokines, and antioxidant enzyme. It also increased the expression of apoptotic genes in spleen and BM. The BP significantly improved hematopoietic function, antioxidant parameters, and serum levels of hematopoietic simulating-cytokines. Also, BP significantly reduced the expression of apoptotic genes. These results confirm the immunomodulatory activity of BP in DOX-induced biochemical, molecular and histological immunosuppression. PRACTICAL APPLICATIONS: Chemotherapy drugs are being developed every day but are limited due to their side effects. The most important side effect of chemotherapy drugs is the suppression of hematopoiesis through its direct effect on bone marrow and hematopoietic cells. Today, many studies are done on natural, synthetic and semi-synthetic compounds to reduce the effects of chemotherapy drugs. Compounds that, along with chemotherapy drugs in the treatment of various tumors, maintain the hematopoietic pathway, synergize the antitumor effects of chemotherapy drugs, and also protect other organs of the body from free radical damage produced by chemotherapy drugs. One of these natural compounds is bee pollen, which has all the properties mentioned in chemotherapy supplements and can be used in the pharmaceutical industry.

Origanum vulgare L. leaves extract alleviates testis and sperm damages induced by finasteride: Biochemical, Immunohistological and apoptosis genes based evidences.

The aim of the current study was to investigate antioxidant, anti-inflammatory and anti-apoptotic effects of Origanum vulgare on finasteride-induced oxidative injury in mouse testis and sperm parameters. Thirty BALB/c mice were divided into 5 groups: negative control, received 0.5 ml/day distilled water; positive control, received 25 mg/kg finasteride orally; and three groups received 100, 200 and 400 mg/kg/day O. vulgare extract plus 25 mg kg-1  day-1 finasteride for 35 days. At day 36, serum luteinising hormone, follicle-stimulating hormone and testosterone, inflammatory cytokines (IL-6, TNF-α, IL-1ß), glutathione peroxidase, superoxide dismutase and nitric oxide levels were assessed. Also, apoptotic changes investigated through genes expression and immunohistochemical staining. Finasteride in 35 days resulted in significant destructive alterations in the testis architecture, suppressed antioxidant enzymes and increased lipid peroxidation. The expression of Bcl-2 was down-regulated, whereas p53 and caspase-3 were up-regulated. Origanum vulgare improved the serum level of hormones and restored the antioxidant defence. 200 and 400 mg/kg/day of O. vulgare alleviated the testis structure and sperm parameters, up-regulated the anti-apoptotic gene Bcl-2 and down-regulated the p53, caspase-3 genes in treated groups. The findings indicate that O. vulgare extract improved function and structure of testis tissue against finasteride-induced testicular toxicity.

The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer's-Like Disease in Rats.

Alzheimer's disease (AD) is a worldwide rapidly growing neurodegenerative disease. Here, we elucidated the neuroprotective effects of silymarin (SM) on the hippocampal tissues of aluminum chloride (AlCl3)-induced Alzheimer-like disease in rats using biochemical, histological, and ultrastructural approaches. Forty rats were divided into control, SM, AlCl3, and AlCl3 + SM groups. Biochemically, AlCl3 administration resulted in marked elevation in levels of lipid peroxidation (LPO) and nitric oxide (NO) and decrease in levels of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Moreover, AlCl3 significantly increased tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1ß), and acetylcholinesterase (AChE) activities. Furthermore, myriad histological and ultrastructural alterations were recorded in the hippocampal tissues of AlCl3-treated rats represented as marked degenerative changes of pyramidal neurons, astrocytes, and oligodendrocytes. Additionally, some myelinated nerve fibers exhibited irregular arrangement of their myelin coats, while the others revealed focal degranulation of their myelin sheaths. Severe defects in the blood-brain barrier (BBB) were also recorded. However, co-administration of SM with AlCl3 reversed most of the biochemical, histological, and ultrastructural changes triggered by AlCl3 in rats. The results of the current study indicate that SM can potentially mend most of the previously evoked neuronal damage in the hippocampal tissues of AlCl3-kindled rats.