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The protective effect of N-acetylcysteine (NAC) and genistein (GEN) on an experimental model of indomethacin (IND)-induced gastric injury was investigated. A total of 50 male rats were divided into 5 groups: (1) control, (2) IND, (3) NAC pretreated, (4) GEN pretreated, and (5) NAC+GEN pretreated. Rats in groups 3-5 were orally administered NAC (500 mg/kg), GEN (10 mg/kg), or both, respectively, once daily for 7 days before the induction of gastric injury by IND (50 mg/kg). The stomach was removed for biochemical analysis and histopathological examination. Pretreatment with NAC, GEN, or both significantly improved ulcer indices and increased nitric oxide level and superoxide dismutase activity. They also significantly decreased malondialdehyde, tumour necrosis factor α levels, and myeloperoxidase activity, and downregulated matrix metalloproteinase 9 (MMP-9) gene expression compared to the IND group. NAC alone ameliorated IND-induced apoptosis, whereas GEN only significantly increased prostaglandin E level. Further, coadministration of both resulted in a significantly better gastroprotective effect versus solo administration. Coadministration of NAC and GEN has an additive gastroprotective effect in IND-induced gastric injury, which may be through interaction of their potential cytoprotective, antioxidant, anti-inflammatory, and antiapoptotic mechanisms together with regulation of MMP-9 expression.

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Multiple sclerosis (MS) is considered to be an autoimmune disorder of the central nervous system (CNS) manifested by chronic inflammation. Although its etiology is not completely understood, inflammation and apoptosis are known to be major players involved in its pathogenesis. Luteolin, the naturally occurring flavonoid, is known by strong antioxidant and anti‐inflammatory properties, yet research studies about its therapeutic role in MS are still lacking. The study aimed to provide insight into effects of luteolin in experimental autoimmune encephalomyelitis (EAE) by monitoring inflammatory, apoptotic, and antioxidant biochemical parameters in addition to histological examination findings. The study included 45 adult female Wistar rats allocated to three equal groups: (a) group I: control group, (b) group II: EAE group, EAE was induced by single intradermal injection of 0.2 mL inoculum comprising 20‐μg recombinant rat myelin oligodendrocyte glycoprotein (MOG), and (c) group III: luteolin‐treated EAE group, luteolin was given in a dose of 10 mg/kg/day, i.p. All groups were subjected to assessment of brain ciliary neurotropic factor (CNTF) mRNA gene expression and measurement of cleaved caspase 3, nuclear factor kappa B (NF‐κB), cyclic AMP (cAMP), and macrophage inflammatory protein 1 alpha (MIP‐1α) by the ELISA technique, total antioxidant capacity (TAC) level is assessed spectrophotometrically. Compared with the EAE group, luteolin‐treated EAE group showed upregulation of CNTF expression and significant increase in cAMP and TAC levels, while it showed significant decrease in cleaved caspase 3, NF‐κB, and MIP‐1α levels. Based on our data herein, luteolin may provide a promising preclinical therapeutic line in MS being anti‐inflammatory, antiapoptotic, and neurotrophic agent. © 2019 IUBMB Life, 71(9):1401–1408, 2019

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Diabetes mellitus (DM) represents a widespread metabolic disease with a well-known neurotoxicity in both central and peripheral nervous systems. Oxymatrine is a traditional Chinese herbal medicine that has various pharmacological activities including; antioxidant, anti-apoptotic and anti-in ammatory potentials. The present work aimed to study the impact of diabetes mellitus on the cerebellar cortex of adult male albino rat and to evaluate the potential protective role of oxymatrine using different histological methods. Fifty-ve adult male rats were randomly divided into three groups: group I served as control, group II was given oxymatrine (80 mg/kg/day) orally for 8 weeks and group III was given a single dose of streptozotocin (50mg/kg) intaperitoneally to induce diabetes. Then diabetic rats were subdivided into two subgroups: subgroup IIIa that received no additional treatment and subgroup IIIb that received oxymatrine similar to group II. The diabetic group revealed numerous changes in the Purkinje cell layer in the form of multilayer arrangement of Purkinje cells, shrunken cells with deeply stained nuclei as well as focal loss of the Purkinje cells. A signi cant increment in GFAP and synaptophysin expression was reported. Transmission electron microscopy showed irregularity and splitting of myelin sheaths in the molecular layer, dark shrunken Purkinje cells with ill-de ned nuclei, dilated Golgi saccules and dense granule cells with irregular nuclear outlines in the granular layer. In contrast, these changes were less evident in diabetic rats that received oxymatrine. In conclusion, Oxymatrine could protect the cerebellar cortex against changes induced by DM.

Diabetes mellitus (DM) represents a widespread metabolic disease with a well-known neurotoxicity in both central and peripheral nervous systems. Oxymatrine is a traditional Chinese herbal medicine that has various pharmacological activities including; anti-oxidant, anti-apoptotic and anti-inflammatory potentials. The present work aimed to study the impact of diabetes mellitus on the cerebellar cortex of adult male albino rat and to evaluate the potential protective role of oxymatrine using different histological methods. Fifty-five adult male rats were randomly divided into three groups: group I served as control, group II was given oxymatrine (80 mg/kg/day) orally for 8 weeks and group III was given a single dose of streptozotocin (50mg/kg) intaperitoneally to induce diabetes. Then diabetic rats were subdivided into two subgroups: subgroup IIIa that received no additional treatment and subgroup IIIb that received oxymatrine similar to group II. The diabetic group revealed numerous changes in the Purkinje cell layer in the form of multilayer arrangement of Purkinje cells, shrunken cells with deeply stained nuclei as well as focal loss of the Purkinje cells. A significant increment in GFAP and synaptophysin expression was reported. Transmission electron microscopy showed irregularity and splitting of myelin sheaths in the molecular layer, dark shrunken Purkinje cells with ill-defined nuclei, dilated Golgi saccules and dense granule cells with irregular nuclear outlines in the granular layer. In contrast, these changes were less evident in diabetic rats that received oxymatrine. In conclusion, Oxymatrine could protect the cerebellar cortex against changes induced by DM.