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Although several treatments are available for the treatment of type 2 diabetes mellitus, adverse effects and cost burden impose the search for safe, efficient, and cost-effective alternative herbal remedies. Syzygium aqueum (Burm.f.) Alston, a natural anti-inflammatory, antioxidant herb, may suppress diabetes-associated inflammation and pancreatic beta-cell death. Here, we tested the ability of the bioactive leaf extract (SA) to prevent streptozotocin (STZ)-induced oxidative stress and inflammation in pancreatic beta cells in rats and the involvement of the TLR-4 signaling pathway. Non-fasted rats pretreated with 100 or 200 mg kg−1 SA 2 days prior to the STZ challenge and for 14 days later had up to 52 and 39% reduction in the glucose levels, respectively, while glibenclamide, the reference standard drug (0.5 mg kg−1), results in 70% reduction. Treatment with SA extract was accompanied by increased insulin secretion, restoration of Langerhans islets morphology, and decreased collagen deposition as demonstrated from ELISA measurement, H and E, and Mallory staining. Both glibenclamide and SA extract significantly decreased levels of TLR-4, MYD88, pro-inflammatory cytokines TNF-α, and TRAF-6 in pancreatic tissue homogenates, which correlated well with minimal pancreatic inflammatory cell infiltration. Pre-treatment with SA or glibenclamide decreased malondialdehyde, a sensitive biomarker of ROS-induced lipid peroxidation, and restored depleted reduced glutathione in the pancreas. Altogether, these data indicate that S. aqueum is effective in improving STZ-induced pancreatic damage, which could be beneficial in treating type 2 diabetes mellitus.

Background: Methotrexate (MTX) is a chemotherapy drug associated with cognitive insufficiency in cancer patients treated with chemotherapy.. Alpha lipoic acid (ALA) has been referred to as the "universal antioxidant" because of its unique antioxidant properties. Aim: To inspect the effect of MTX on the hippocampus and to correlate them with the cognition impairment and to assess the practical neuroprotective role of ALA on hippocampus. Material and Method: Thirty two male adult albino were classified into four groups: control group (Physiologic saline), ALA group: (200 mg/kg orally for three weeks), MTX group: (250 mg/ kg) as a single dose intraperitoneally injected and MTX +ALA group: rats were administrated a single dose of intraperitoneal injection of MTX (250 mg/ kg) in the fourth day and were given ALA in a dose of 200 mg/kg orally for three weeks starting from the first day. All animals were subjected to Morris Water Maze testing to assess the hippocampus functions. At the end of the experiment, all animals anesthetized, cerebrum removed and the specimen subjected to histological procedures and biochemical examination. Results: MTX caused impaired performance of Morris Water Maze of rats and biochemical changes significant decrease in oxidative enzymes and increase in malondialdehyde (MDA) tissue levels. Moreover, MTX caused histological changes in rat hippocampus in the form of degenerative and apoptotic neurons which confirmed by immnnohistochemical staining of caspase-3 and GFAP staining and morphometrical analysis of pyramidal cell layer thickness and pyramidal cell count. Co-administration of ALA with MTX significantly diminished the behavioral affection and biochemical changes in rat treated with MTX and ameliorated the histological changes of hippocampus tissue. Conclusion: Our experimental results proved the harmful effect of MTX on hippocampus tissue that explained the cognitive impairment that associated with MTX and confirm the antioxidant and the antiapoptotic properties of ALA on hippocampus tissue.

Background: The hippocampus is a major component of the mammalian brains and the brains of other vertebrates. It belongs to the limbic system and plays important roles in memory consolidation. Methotrexate (MTX) belongs to the antimetabolite group, which is an antineoplastic group of drugs. MTX has a wide range of therapeutic effects: e.g. at high doses in many malignancies and at low doses in autoimmune diseases such as rheumatoid arthritis and psoriasis, due to its anti-inflammatory and immunosuppressive effects. The therapeutic actions of Alpha Lipoic Acid (ALA) is based on its antioxidant properties including its capacity in regenerating endogenous antioxidants, its metal chelating abilities, its action as a scavenger of reactive oxygen species (ROS) and its capability to repair oxidative damage. Objective: This work aimed to study the neurotoxic effects of methotrxate (MTX) on rat hippocampus and to explore the neuroprotective role of alpha lipoic acid (ALA). Methods: The databases were searched for articles published in English in 4 data bases [PubMed -Google scholar-Science direct and Egyptian bank of knowledge] and Boolean operators (and, or, not) had been used such as neurotoxic effects of methotrxate and rat hippocampus OR alpha lipoic acid and in reviewed articles. Conclusion: So, from this review article, it can be concluded that, alpha lipoic acid administration along with methotrxate therapy can ameliorate the harmfull effects of methotrxate on hippocampus.