Antidiabetic Evaluation of Kigelia pinnata Root Bark Extract in Streptozotocin-Induced Type-2 Diabetes Model of Rats.

Diabetes mellitus (DM) is the most common endocrine disorder characterized by increased blood glucose levels resulting from defective insulin secretion, resistance to insulin action, or both. DM is often associated with severe complications, and there is an increasing appreciation that cognitive function declines in DM. The aim of this research work was to evaluate Kigelia pinnata root bark extract in Streptozotocin (STZ)-induced type-2 diabetes. Experimental diabetes was induced by a single administration of STZ (60 mg/kg, intraperitoneal [i.p.]), immediately after the STZ administration, and all animals were fed with normal food and water. Nicotinamide was administered (120 mg/kg, i.p.) 15 min before STZ. The development of hyperglycemia was confirmed by the elevated blood glucose levels determined at fixed intervals, which was confirmed by measuring fasting blood glucose levels in rats' blood taken from the tail vein. Supplementation with ethanolic extract of K. pinnata root bark (EEKP) significantly reduced the elevated blood glucose in STZ-induced hyperglycemia in rats. EEKP significantly restored the biochemical and antioxidant defense system. On the final day of the protocol, the extract also reduced inflammatory cytokines in the blood serum.

Syringic acid alleviates valproic acid induced autism via activation of p38 mitogen-activated protein kinase: Possible molecular approach.

Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental disorder characterized by restrictive and repetitive behavior followed by impairment in social, verbal, and non-verbal interaction and communication. Valproic acid (VPA) is a well-known anti-epileptic drug, but its prenatal exposure to animals causes social impairment, neurotransmitters imbalance, and neuroinflammation with ASD-like phenotypes. Syringic acid (SA) is a polyphenolic compound with anti-inflammatory, anti-apoptotic, antioxidant, and neuromodulator activity. The purpose of study was to investigate the protective effect of Syringic acid (SA) in prenatal VPA-treated rats through behavioral, neuroinflammation, oxidative stress, neurotransmitters, neuronal integrity, and apoptotic marker. Single dose of VPA was administered 600 mg/kg, i.p. on a gestational day (GD) 12th and SA was administrated from PnD 26th to 54th at the dose of 25, 50, and 100 mg/kg, p.o. On PnD 56th behavioral parameters (Pain sensitivity, open field test, narrow beam walks test and social impairment test) were performed and all animals were sacrificed, and brain tissue was isolated for oxidative stress (GSH, CAT, and LPO), neuroinflammation (TNF-α and IL-6) and neurotransmitters (GABA and Glutamate), histopathology (H&E, Nissl), immunohistochemistry (p38 MAPK) analysis. Rat treated with SA dose-dependently prevented behavioral alteration, restored antioxidant enzymes, neurotransmitters level, decreased neuroinflammatory markers, and improved neuronal integrity. Furthermore, immunohistochemistry confirmed the reduced p38 MAPK marker expression by SA in VPA induced autistic behavior.

Microbiota- Brain-Gut-Axis Relevance to Parkinson's Disease: Potential Therapeutic Effects of Probiotics.

Parkinson's disease (PD) is the second most common type of neurogenerative disease among middleaged and older people, characterized by aggregation of alpha-synuclein and dopaminergic neuron loss. The microbiota- gut-brain axis is a dynamic bidirectional communication network and is involved in the pathogenesis of PD. The aggregation of misfolded protein alpha-synuclein is a neuropathological characteristic of PD, originates in the gut and migrates to the central nervous system (CNS) through the vagus nerve and olfactory bulb. The change in the architecture of gut microbiota increases the level short-chain fatty acids (SCFAs) and other metabolites, acting on the neuroendocrine system and modulating the concentrations of gamma-Aminobutyric acid (GABA), serotonin, and other neurotransmitters. It also alters the vagus and intestinal signalling, influencing the brain and behaviour by activating microglia and systemic cytokines. Both experimental and clinical reports indicate the role of intestinal dysbiosis and microbiota host interaction in neurodegeneration. Probiotics are live microorganisms that modify the gut microbiota in the small intestine to avoid neurological diseases. Probiotics have been shown in clinical and preclinical studies to be effective in the treatment of PD by balancing the gut microbiota. In this article, we described the role of gut-microbiota in the pathogenesis of PD. The article aims to explore the mechanistic strategy of the gut-brain axis and its relation with motor impairment and the use of probiotics to maintain gut microbial flora and prevent PD-like symptoms.