This study examined if wheat germ oil (WGO) has gastroprotective impacts against ethanol-induced gastric ulcer in rats. Rats were assigned into control, WGO, ethanol, omeprazole + ethanol, and WGO + ethanol. WGO prevented gastric ulceration and damage induced by ethanol, the same effect induced by omeprazole, a widely known medication used for gastric ulcer treatment. WGO reduced gastric ulcer index, nitric oxide, and malondialdehyde levels in the stomach. WGO boosted the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Bcl2, and the antioxidants. WGO showed inflammatory and anti-inflammatory impacts through the control of interleukin (IL)-1β, Tumor necrosis factor alpha (TNF-α), and IL-10 that were altered in ethanol-administered rats. Ethanol up-regulated caspase-3 and nuclear factor-kappa B (NF-kB) expression and showed histopathological changes such as necrosis and mucosal degeneration that were mitigated by pre-administration of WGO. Moreover, WGO decreased gastric immunoreactivity of NF-kB and increased transforming growth factor beta-1 (TGF-β1) that were associated with upregulation of Nrf2, heme oxygenase-1 (HO-1), and antioxidant expression and production. In conclusion, WGO reduced ethanol-induced stomach toxicity by regulating genes involved in oxidative stress, inflammation, and apoptotic/antiapoptotic pathways.

Gentamicin (GM) is an effective and probably the most commonly used aminoglycosides antibiotic, however the risk of causing nephrotoxicity limits its use. In the present study, the possible protective effects of Saccharum officinarum L. (sugar cane juice) on gentamicin induced acute oxidative renal injury in experimental rats were investigated. Twenty adult albino rats were randomly allocated into four groups (5 rats in each) and treated once daily for a period of 7 days as follows; group A being the negative control and was injected intraperitoneal with normal saline, group B (sugar cane juice treated group) was given sugar cane juice orally at a dose of 15 ml/kg/day, group C (GM treated group) and group D (sugar cane juice + GM treated group) were the experimental groups and were injected intraperitoneal with (80 mg/kg/day GM) & (sugar cane juice 15 ml/kg/day orally + 80 mg/kg/day GM intraperitoneal) respectively. By the end of the experiment, the biochemical kidney functions tests (urinary cystatin C and kidney injury molecule-1, blood urea and creatinine) were investigated. Also, oxidative stress parameters (malondialdehyde [MDA] level, superoxide dismutase [SOD] & glutathione peroxidase [GPX] enzymatic activity) in renal tissue were evaluated. Histopathological examinations of kidney were done to assess the degree of renal protection induced by sugarcane juice, Gentamicin treated rats showed; marked significant rise in the biochemical kidney functions tests and lipid peroxidation (MDA) parameter in renal tissues, along with significant reduction in renal tissue antioxidant enzymatic activity of both SOD & GPX. However, co-administration of sugar cane juice in group D leading to marked reduction in previous biochemical markers and MDA levels together with significant elevated renal SOD &GPX enzymatic activity which nearly tend to return to normal values. The histopathological examination of groups A and B showed normal kidney structure which was deranged in group C (GM treated), whereas group D showed significant recovery in histological structures. Gentamicin induced acute renal injury and oxidative damage. Co-administration of sugar cane juice may reduce this damage by improving antioxidant defense and tissue integrity in experimental albino rats.   

Although the classic form of asthma is characterized by chronic pneumonitis with eosinophil infiltration and steroid responsivity, asthma has multifactorial pathogenesis and various clinical phenotypes. Previous studies strongly suggested that chemical exposure could influence the severity and course of asthma and reduce its steroid responsiveness. Cypermethrin (CYP), a common pesticide used in agriculture, was investigated for the possible aggravation of the ovalbumin (OVA)-induced allergic pneumonitis and the possible induction of steroid resistance in rats. Additionally, it was investigated whether pirfenidone (PFD) could substitute dexamethasone, as an alternative treatment option, for the induced steroid resistance. Fifty-six male Wistar albino rats were randomly divided into seven groups: control, PFD alone, allergic pneumonitis, CYP alone, allergic pneumonitis/CYP-exposed, allergic pneumonitis/CYP/dexamethasone (Dex), and allergic pneumonitis/CYP/PFD-treated groups. Allergic pneumonitis was induced by three intraperitoneal OVA injections administered once a week, followed by an intranasal OVA instillation challenge. CYP (25 mg/kg/d), Dex (1 mg/kg/d), and PFD (100 mg/kg/d) were administered orally from day 15 to the end of the experiment. Bronchoalveolar lavage fluid (BALF) was analyzed for cytokine levels. Hematoxylin and eosin (H&E) and periodic acid Schiff (PAS)-stained lung sections were prepared. Immunohistochemical identification of p38 MAPK and lung macrophages was performed. The inflammatory/oxidative status of the lung and PCR-quantification of the STAT6, p38 MAPK, MUC5AC, and IL-13 genes were carried out. The allergic pneumonitis-only group showed eosinophil-mediated inflammation (p < 0.05). Further CYP exposure aggravated lung inflammation and showed steroid-resistant changes, p38 activation, neutrophil-mediated, M1 macrophage-related inflammation (p < 0.05). All changes were reversed (p < 0.05) by PFD, meanwhile not by dexamethasone treatment. Pirfenidone could replace dexamethasone treatment in the current rat model of CYP-induced severe steroid-resistant asthma via inhibiting the M1 macrophage differentiation through modulation of the STAT6/p38 MAPK pathway.