In vivo and computational investigation of butin against alloxan-induced diabetes via biochemical, histopathological, and molecular interactions.

Herbs have been used as medicines since antiquity, and it has been discovered that the human body responds well to herbal remedies. Research on the effect of butin was conducted in the current study in the alloxan-induced diabetic rat paradigm. A total of 30 Wistar rats were randomly assigned into the following groups (n = 6): I-Normal; II-Alloxan-induced (50 mg/kg); III-Alloxan + butin 25 mg/kg; IV-Alloxan + butin 50 mg/kg; V-Butin per se 50 mg/kg. Various diabetic parameters (blood glucose, insulin, HbA1c), lipid profile, inflammatory (TNF-α, IL-1ß, IL-6 and NF-κB), antioxidant enzymes (CAT, SOD and GSH), oxidative stress indicators (MDA), apoptosis marker (caspase-3), hepatic markers (ALT and AST), and histopathological changes were assessed. Additionally, molecular docking and dynamics were performed to evaluate the interaction of butin with target proteins. Butin treatment, at both doses, significantly restored biochemical parameters and preserved pancreatic histopathology in diabetic rats. It effectively modulated blood parameters, lipid profiles, inflammatory markers, apoptosis, antioxidant enzyme activity, oxidative stress, and hepatic markers. Molecular docking revealed that butin binds to proteins such as caspase-3 (1NME), NF-κB (1SVC), and serum insulin (4IBM) with binding affinities of - 7.4, - 6.5, and - 8.2 kcal/mol, respectively. Molecular dynamics simulations further suggested that butin induces significant conformational changes in these proteins. Butin exhibits potential effects against alloxan-induced diabetic rats by restoring biochemical balance, reducing inflammation, and protecting pancreatic tissue. Its binding to key proteins involved in apoptosis and inflammation highlights its therapeutic potential in diabetes management.

6-shogaol against 3-Nitropropionic acid-induced Huntington's disease in rodents: Based on molecular docking/targeting pro-inflammatory cytokines/NF-κB-BDNF-Nrf2 pathway.

BACKGROUND: Huntington's disease (HD) is an extremely harmful autosomal inherited neurodegenerative disease. Motor dysfunction, mental disorder, and cognitive deficits are the characteristic features of this disease. The current study examined whether 6-shogaol has a protective effect against 3-Nitropropionic Acid (3-NPA)-induced HD in rats. METHODS: A total of thirty male Wistar rats received 6-shogaol (10 and 20 mg/kg, per oral) an hour before injection of 3-NPA (10 mg/kg i.p.) for 15 days. Behavioral tests were performed, including narrow beam walk, rotarod test, and grip strength test. Biochemical tests promoting oxidative stress were evaluated [superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT) and malondialdehyde (MDA)], including changes to neurotransmitters serotonin (5-HT), dopamine (DA), norepinephrine (NE), homovanillic acid (HVA), (3,4-dihydroxyphenylacetic acid (DOPAC), γ-aminobutyric acid (GABA), and 5-hydroxy indole acetic acid (5-HIAA), nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), interleukins-1ß (IL-1ß), IL-6, brain-derived neurotrophic factor (BDNF), and nuclear factor erythroid 2-related factor 2 (Nrf2). The 6-shogaol was docked to the active site of TNF-α (2AZ5), NF-κB (1SVC), BDNF) [1B8M], and Nrf2 [5FZN] proteins using AutoDock tools. RESULTS: The 6-shogaol group significantly improved behavioral activity over the 3-NPA-injected control rats. Moreover, 3-NPA-induced significantly altered neurotransmitters, biochemical and neuroinflammatory indices, which could efficiently be reversed by 6-shogaol. The 6-shogaol showed favorable negative binding energies at -9.271 (BDNF) kcal/mol. CONCLUSIONS: The present investigation demonstrated the neuroprotective effects of 6-shogaol in an experimental animal paradigm against 3-NPA-induced HD in rats. The suggested mechanism is supported by immunohistochemical analysis and western blots, although more research is necessary for definite confirmation.

Barbaloin Protects Pentylenetetrazol-Induced Cognitive Deficits in Rodents via Modulation of Neurotransmitters and Inhibition of Oxidative-Free-Radicals-Led Inflammation.

BACKGROUND: Epilepsy is defined by an excessive level of activity in the neurons and coordinated bursts of electrical activity, resulting in the occurrence of seizure episodes. The precise cause of epileptogenesis remains uncertain; nevertheless, the etiology of epilepsy may involve neuroinflammation, oxidative stress, and malfunction of the neurotransmitter system. OBJECTIVE: The goal of this investigation was to assess barbaloin's protective properties with respect to pentylenetetrazol (PTZ)-)-induced cognitive deficits in rats via antioxidative, anti-inflammatory, and neurotransmitter-modulating effects. METHODS: Wistar rats were subjected to PTZ [40 mg/kg (i.p.)], which induced cognitive decline. Behavior assessment using a kindling score, open-field test (OFT), novel object recognition test (NORT), and assays for superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT), malondialdehyde (MDA), acetylcholinesterase (AChE), caspase-3, nitric oxide (NO), interleukins-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), IL-6, nuclear factor kappa-B (NF-κB), Bcl-2 and Bax, and neurotransmitter levels [GABA, DA, NE, and serotonin (5-HT)] were performed. RESULTS: The treatment of rats with barbaloin resulted in behavior improvement and significant changes in the levels of GSH, SOD, CAT, MDA, AChE, NO, IL-6, IL-1ß, TNF-α, NF-κB, caspase-3, Bcl-2, and Bax compared to the PTZ control group. Barbaloin treatment resulted in notable changes in neurotransmitter levels (GABA, NE, 5-HT, DA) compared to the PTZ group. CONCLUSIONS: The ongoing study has gathered evidence indicating that the injection of barbaloin has resulted in significant improvements in cognitive performance in rats. This is achieved by inhibiting oxidative stress, enhancing the activity of natural antioxidant enzymes, reducing cytokine levels, and increasing the levels of neurotransmitters in the brain. These results were detected in comparison to a PTZ control and can be attributed to the potent anti-inflammatory and antioxidant capabilities of barbaloin, which could be linked to its neuroprotective properties. Barbaloin may potentially increase cognitive decline and boost neuronal survival by altering the expression of Bax, caspase-3, Bcl-2.

Europinidin Attenuates Methamphetamine-induced Learning and Memory Impairments and Hippocampal Alterations in Rodents: Based on Molecular Docking through a Mechanism of Neuromodulatory Cytokines/ Caspases-3/ CREB/BDNF Pathway.

BACKGROUND: Methamphetamine (MA) is well recognized as a psychostimulant that can cause neurotoxicity and neurodegeneration, which is associated with cognitive decline, has been confirmed experimentally. OBJECTIVE: The research aimed to investigate the neuroprotective properties of europinidin (Eu) in rodents affected by methamphetamine (MA)-induced cognitive impairments and hippocampal alterations. This was achieved by inhibiting lipid peroxidation and pro-inflammatory markers. METHODS: Rats were exposed to cognitive impairment produced by MA. The Morris water maze (MWM) is utilized for evaluating behavioral parameters. Tests were conducted on malondialdehyde (MDA), catalase (CAT), interleukins-1ß (IL-1ß), reduced glutathione (GSH), tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD), and the expression of neurotransmitters (Norepinephrine [NE], dopamine [DA], glutamate, and gamma-aminobutyric acid [GABA]) as well as cAMP response element-binding protein (CREB), IL-6, brain-derived neurotrophic factor (BDNF), and caspase 3 proteins. An investigation was carried out using docking methodology to ascertain whether Eu interacts with relevant molecular targets. RESULTS: Significant decline in the transfer latency and there were significant changes in the amount of SOD, GSH, CAT, and MDA and alterations in levels of IL-6, IL-1ß, CREB, TNF-α, BDNF, and Caspase 3 proteins expression, as well as considerably alterations in level of neurotransmitters (NE, DA, Glutamate, and GABA) were observed in the Eu-treated rats compared to the MA-induced rats. Eu had a favorable affinity towards BDNF with docking scores of -9.486 kcal/mol. CONCLUSION: The experiment found that administering Eu to rats improved cognitive abilities by changing antioxidant enzymes, reducing cytokines, and modifying neurotransmitter levels, compared to rats in the control group treated with MA.

Hibiscetin attenuates lipopolysaccharide-evoked memory impairment by inhibiting BDNF/caspase-3/NF-κB pathway in rodents.

This study explores the neuroprotective potential of hibiscetin concerning memory deficits induced by lipopolysaccharide (LPS) injection in rats. The aim of this study is to evaluate the effect of hibiscetin against LPS-injected memory deficits in rats. The behavioral paradigms were conducted to access LPS-induced memory deficits. Various biochemical parameters such as acetyl-cholinesterase activity, choline-acetyltransferase, antioxidant (superoxide dismutase, glutathione transferase, catalase), oxidative stress (malonaldehyde), and nitric oxide levels were examined. Furthermore, neuroinflammatory parameters such as tumor necrosis factor-α, interleukin-1ß (IL-1ß), IL-6, and nuclear factor-kappa B expression and brain-derived neurotrophic factor as well as apoptosis marker i.e., caspase-3 were evaluated. The results demonstrated that the hibiscetin-treated group exhibited significant recovery in LPS-induced memory deficits in rats by using behavioral paradigms, biochemical parameters, antioxidant levels, oxidative stress, neuroinflammatory markers, and apoptosis markers. Recent research suggested that hibiscetin may serve as a promising neuroprotective agent in experimental animals and could offer an alternative in LPS-injected memory deficits in rodent models.

Review of the potential pharmacological role of erucic acid: a monounsaturated omega-9 fatty acid.

This comprehensive review aims to provide an overview of the pharmacological properties of erucic acid (EA) and highlight areas that require further research. EA is an omega-9 fatty acid found in certain vegetable oil, such as rapeseed oil has demonstrated favourable effects in rodents, including ameliorating myocardial lipidosis (fat accumulation in the heart muscle), congestive heart disease, hepatic steatosis (fat accumulation in the liver), and memory impairments. These findings have prompted regulatory bodies to establish limits on EA content in food oils. The studies were performed on rodents and led to caution on ingesting the EA at high levels. Moreover, EA is frequently utilized as a nutritional supplement for the treatment of adrenoleukodystrophy, myocardial disease, and memory improvement. The review of the article indicated that EA improves cognitive function, has a part in Huntington's disease, interacts with peroxisome proliferator-activated receptors, inhibits elastase and thrombin, has anti-inflammatory, antioxidant, and anti-tumour properties, and inhibits influenza A virus. This article elucidates the pharmacological effects of EA, an omega-9 fatty acid.

Influence of rosiridin on streptozotocin-induced diabetes in rodents through endogenous antioxidants-inflammatory cytokines pathway and molecular docking study.

The research was undertaken to assess the antidiabetic activity of rosiridin in the streptozotocin (STZ)-induced diabetic model. Type 2 diabetes mellitus was elicited chemically in experimental animals using STZ (60 mg/kg, i.p.). Experimental rats were arbitrarily allocated to normal control, rosiridin perse, diabetic control, and STZ + rosiridin groups. After the confirmation of diabetes, rosiridin (10 mg/kg) was given orally to the experimental animals for 30 days. Various anti-diabetic (blood glucose, insulin), hypolipidemic, anti-inflammatory (Nuclear factor kappa B, tumour necrosis factor-α, interleukin beta (IL-1ß), and IL-6), antioxidant (and malondialdehyde level, hepatic function and others markers (ALT, AST, adiponectin, and FNDC5) and histopathological indices of injury were evaluated. In addition, the rosinidin was docked into the active site of NF-Kß (1SVC), FNDC5 (4LSD) and adiponectin (5LXG) proteins with AutoDock tools. MD simulations were carried out for the complexes of rosiridin with NF-Kß, myokine and human adiponectin receptor 1. Rosiridin treatment restored the biochemical parameters and preserved the histopathological building of the pancreas as compared to the diabetic rats. Histopathological analysis of the pancreas confirmed that rosiridin antidiabetic efficacy in the STZ-induced diabetes mellitus model. The 5LXG_rosinidin showed favourable affinity with the best binding energies at -7.534 kcal/mol. MD simulations were carried out for the complexes of rosiridin with NF-Kß, myokine and human adiponectin receptor 1, the complex of myokine and rosiridin exhibited the most stable complex. Rosiridin may exhibit considerable anti-diabetic activity in the STZ-induced diabetes mellitus model.Communicated by Ramaswamy H. Sarma.

Acemannan ameliorates STZ-activated diabetes by attenuating high glucose via inhibiting inflammatory cytokines and apoptosis pathway.

Acemannan, the main polysaccharide in Aloe vera, is a -(1, 4)-acetylated polymannose. According to numerous research findings, acemannan is a viable alternative for the treatment of pathological disorders. Streptozotocin (STZ, 60 mg/kg) administered intraperitoneally caused type 2 diabetes in rats. The current study sought to determine the anti-diabetic efficacy of acemannan (25 and 50 mg/kg) in STZ-injected rats. Different biochemical parameters including HbA1C, glucose and serum insulin, lipid profile, inflammatory markers, antioxidant, oxidative balance, liver function test, glycogen and creatinine, and caspase-3 were evaluated. In addition, a molecular docking study was performed to estimate acemannan's binding affinity to inflammatory markers. Acemannan may be a potent anti-diabetic agent for the treatment of diabetic patients, which will aid in future research into alternative diabetes medications.

Effect of Europinidin against Alcohol-Induced Liver Damage in Rats by Inhibiting the TNF-α/TGF-ß/IFN-γ/NF-kB/Caspase-3 Signaling Pathway.

BACKGROUND: The effect of europinidin on alcoholic liver damage in rats was examined in this research. METHODS: A total of 24 Wistar rats were grouped in the same way into four groups: normal control (normal), ethanol control (EtOH), europinidin low dose (10 mg/kg), and europinidin higher dose (20 mg/kg). The test group rats were orally treated with europinidin-10 and europinidin-20 for 4 weeks, whereas 5 mL/kg distilled water was administered to control rats. In addition, 1 h after the last dose of the above-mentioned oral treatment, 5 mL/kg (i.p.) EtOH was injected to induce liver injury. After 5 h of EtOH treatment, samples of blood were withdrawn for biochemical estimations. RESULTS: Administration of europinidin at both doses restored all of the estimated serum, i.e., liver function tests (ALT, AST, ALP), biochemical test (Creatinine, albumin, BUN, direct bilirubin, and LDH), lipid assessment (TC and TG), endogenous antioxidants (GSH-Px, SOD, and CAT), malondialdehyde (MDA), nitric oxide (NO), cytokines (TGF-ß, TNF-α, IL-1ß, IL-6, IFN-γ, and IL-12), caspase-3, and nuclear factor kappa B (NF-κB) associated with the EtOH group. CONCLUSION: The results of the investigation showed that europinidin had favorable effects in rats given EtOH and may have hepatoprotective potential property.

Protective effect of fustin against adjuvant-induced arthritis through the restoration of proinflammatory response and oxidative stress.

Rheumatoid arthritis causes irreparable damage to joints. The present research sought to check fustin's anti-arthritic efficacy against the complete Freund's adjuvant-induced arthritis paradigm in animals by altering the inflammatory response. In the rats, complete Freund's adjuvant was used to trigger arthritis and they received fustin at 50 and 100 mg/kg for 21 days. At regular intervals, the hind paw volume and arthritic score were assessed. After the trial period, hematological, antioxidant, pro-inflammatory cytokines, and other biochemical parameters were estimated. Fustin-treated rats showed the down-regulation of hind paw volume, arthritic score, and altered hematological parameters (TLC, DLC (neutrophil, lymphocyte, monocyte, eosinophil, basophil)). Furthermore, fustin significantly mitigates proinflammatory cytokine (reduced interleukin, tumor necrosis factor-a (TNF-α), IL-6, IL-1ß), oxidative stress (attenuated malondialdehyde (MDA), catalase (CAT), glutathione (GSH), superoxide dismutase (SOD)), attenuated production of prostaglandin E2 and myeloperoxidase (MPO) and improved nuclear factor erythroid 2-related factor (Nrf2) action. Fustin led to the benefit in arthritis-prone animals elicited by complete Freund's adjuvant via pro-inflammatory cytokine.

Protective Effect of Hirsutidin against Rotenone-Induced Parkinsonism via Inhibition of Caspase-3/Interleukins-6 and 1ß.

A participant of the chemical family recognized as anthocyanins, hirsutidin is an O-methylated anthocyanidin. It is a natural substance, i.e., existing in Catharanthus roseus (Madagascar periwinkle), the predominant component in petals, as well as callus cultures. The literature review indicated a lack of scientifically verified findings on hirsutidin's biological activities, particularly its anti-Parkinson's capabilities. Using the information from the previous section as a reference, a present study has been assessed to evaluate the anti-Parkinson properties of hirsutidin against rotenone-activated Parkinson's in experimental animals. For 28 days, rats received hirsutidin at a dose of 10 mg/kg and rotenone at a dose of 0.5 mg/kg s.c. to test the neuroprotective effects. The hirsutidin was given 1 h before the rotenone. Behavioral tests, including the rotarod test, catalepsy, Kondziela's inverted screen activity, and open-field analysis, were performed. The levels of neurotransmitters (5-HT, DOPAC, 5-HIAA, dopamine, and HVA), neuroinflammatory markers (TNF-α, IL-6, IL-1ß, caspase-3), an endogenous antioxidant, nitrite content, and acetylcholine were measured in all the rats on the 29th day. Hirsutidin exhibited substantial behavioral improvement in the rotarod test, catalepsy, Kondziela's inverted screen activity, and open-field test. Furthermore, hirsutidin restored neuroinflammatory markers, cholinergic function, nitrite content, neurotransmitters, and endogenous antioxidant levels. According to the study, hirsutidin has anti-inflammatory and antioxidant characteristics. As a result, it implies that hirsutidin may have anti-Parkinsonian effects in rats.

Neuroprotectant Effects of Hibiscetin in 3-Nitropropionic Acid-Induced Huntington's Disease via Subsiding Oxidative Stress and Modulating Monoamine Neurotransmitters in Rats Brain.

BACKGROUND: Previously reported data suggest that hibiscetin, isolated from roselle, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD). METHODS: To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups (n = 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1ß), and myeloperoxidase (MPO) were evaluated. RESULTS: The hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin. CONCLUSION: The current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models.

Protective Effect of Fustin against Huntington's Disease in 3-Nitropropionic Treated Rats via Downregulation of Oxidative Stress and Alteration in Neurotransmitters and Brain-Derived Neurotrophic Factor Activity.

Researchers have revealed that Rhus verniciflua heartwood, which contains fustin as an important component, possesses antioxidant-mediated, anti-mutagenic, and anti-rheumatoid arthritis characteristics. Additionally, out of the numerous plant-derived secondary metabolites, there are various research papers concentrating on flavonoids for potential advantages in neurological illnesses. The current study aims to assess the neuroprotective potential of fustin in rodents over 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD)-like consequences. The efficacy of fustin 50 and 100 mg/kg was studied with multiple-dose administrations of 3-NPA, which experimentally induced HD-like symptoms in rats for 22 days. At the end of the study, several behavioral tests were performed including a beam walk, rotarod, and grip strength tests. Similarly, some biochemical parameters were assessed to support oxidative stress (reduced glutathione-GSH, superoxide dismutase-SOD, catalase-CAT, and malondialdehyde-MDA), alteration in neurotransmitters (gamma-aminobutyric acid-GABA-and glutamate), alteration in brain-derived neurotrophic factor activity, and nitrite levels. Additionally, pro-inflammatory parameters were carried out to evaluate the neuroinflammatory responses associated with streptozotocin such as TNF-α, IL-1ß, and COX in the perfused brain. The fustin-treated group exhibited a significant restoration of memory function via modulation in behavioral activities. Moreover, 3-NPA altered biochemical, neurotransmitters, brain protein levels, and neuroinflammatory measures, which fustin efficiently restored. This is the first report demonstrating the efficacy of novel phytoconstituent fustin as a potential future candidate for the treatment of HD via offering neuroprotection by subsiding the oxidative and enzymatic activity in the 3-NPA experimental animal paradigm.

Effects of the Anthocyanin Hirsutidin on Gastric Ulcers: Improved Healing through Antioxidant Mechanisms.

The goal of this study was to determine the effect of hirsutidin on ethanol-induced stomach ulcers in rats. Rats (n = 24 rats/group) were separated at random into the following groups: normal saline-treated (normal control), ethanol-treated (ethanol control), 10 mg/kg hirsutidin + ethanol-treated (hirsutidin 10), and 20 mg/kg hirsutidin + ethanol-treated (hirsutidin 20). All the groups received the respective treatment orally for 7 days. On day 7, i.e., after 24 h of fasting, except for the normal control group, all the groups orally received 5 mL/kg of ethanol. Four hours later, rats were anaesthetized, serum was isolated from the blood, and biochemical tests were performed. The stomach tissue was utilized for ulcer grading, histology, and biochemical analysis. The rats developed stomach acidity and ulcers after being given ethanol based on increased ulcer score, disturbed cellular architecture, increased oxidative stress, myeloperoxidase and decreased endogenous antioxidants, and nitric oxide and prostaglandin E2 concentration. Ethanol-treated rats also displayed increased tumor necrosis factor-α, aspartate aminotransferase, alanine transaminase, alkaline phosphatase, and inflammatory cytokines. The treatment with hirsutidin protected and significantly restored all serum parameters in ethanol-induced stomach ulcers and may have antiulcer activity.

Rosinidin Protects against Cisplatin-Induced Nephrotoxicity via Subsiding Proinflammatory and Oxidative Stress Biomarkers in Rats.

BACKGROUND: Rosinidin is a flavonoid anthocyanin pigmentation found in shrub flowers such as Catharanthus roseus and Primula rosea. The molecular docking studies predicted that rosinidin has adequate structural competency, making it a viable medicinal candidate for the treatment of a wide range of disorders. The current study intends to assess rosinidin nephroprotective efficacy against nephrotoxicity induced by cisplatin in rats. MATERIALS AND METHODS: Oral acute toxicity tests of rosinidin were conducted to assess potential toxicity in animals, and it was shown to be safe. The nephroprotective effect of rosinidin 10, and 20 mg/kg were tested in rats for 25 days with concurrent administration of cisplatin. Several biochemical parameters were measured to support enzymatic and non-enzymatic oxidative stress such as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH). Likewise, changes in several non-protein-nitrogenous components and blood chemistry parameters were made to support the theory linked with the pathogenesis of chemical-induced nephrotoxicity. RESULTS: Cisplatin caused significant changes in biochemical, enzymatic, and blood chemistry, which rosinidin efficiently controlled. CONCLUSIONS: The present investigation linked rosinidin with nephroprotective efficacy in experimental models.

Protective Effect of Fustin Against Ethanol-Activated Gastric Ulcer via Downregulation of Biochemical Parameters in Rats.

The fustin plant-derived bioflavonoid obtained from a common plant known as lacquer tree from family Anacardiaceae, formally known as Rhus verniciflua Stokes, is known to exert a variety of therapeutic properties. The current investigation proved the anti-ulcerative property of fustin on ethanol-induced gastric ulcers in an experimental animal model. The fustin 50 and 100 mg/kg was studied in an experimental rat model by performing an 8 day protocol. The ulcer index, pH, total acidic content, and biochemical parameters such as glutathione (GSH), superoxide dismutase (SOD), catalase activity (CAT), malondialdehyde (MDA), interleukin-1ß, prostaglandin E-2, tumor necrosis factor-α (TNF-α), myeloperoxidase, and nitric oxide (NO) in serum were measured. The gastric parameter such as ulcer index, pH, and acidic content was maintained in the fustin groups compared to the ethanol control group. Clinical presentation of gastric ulcers includes a significant increase in serum levels, GSH, SOD, and CAT and decreased MDA, TNF-α, interleukin-1ß, and prostaglandin E-2 parameters in contrast to normal groups. The treatment regimen with fustin has significantly restored all serum parameters in test groups. The current study helps to develop reasonable phytochemical options for the innervations of chemical-induced gastric ulcers.

Antiamnesic Potential of Malvidin on Aluminum Chloride Activated by the Free Radical Scavenging Property.

Objectives: Malvidin, a dietary anthocyanin can be a potent drug for the treatment of neuronal toxicity. The investigation was aimed to study the antioxidant role of malvidin against aluminum chloride (AlCl3)-induced neurotoxicity in rats. Methods: To evaluate the neuroprotective role of malvidin, the rats were divided into four different groups: group I received saline, group II received AlCl3, and groups III and IV were administered with 100 and 200 mg/kg malvidin after AlCl3 for 60 days. During the evaluation period, all the groups were subjected to a behavioral test. On the 61st day of the study, rat brains were removed and used for a neurochemical assay. Results: From the present study, malvidin ameliorated the effects of AlCl3 on behavioral parameters. Biochemical investigation revealed that oral treatment of malvidin shows neuroprotective effects through regulation of antioxidant levels and neuroinflammation in the AlCl3-exposed rats. Conclusion: The results indicate that malvidin possesses antioxidant activity via acetylcholinesterase inhibition and regulation of oxidative stress in neuronal cells. Hence, malvidin could be a potential drug in correcting Alzheimer's disease.

Anti-Huntington's Effect of Rosiridin via Oxidative Stress/AchE Inhibition and Modulation of Succinate Dehydrogenase, Nitrite, and BDNF Levels against 3-Nitropropionic Acid in Rodents.

Background: Rosiridin is a compound extracted from Rhodiola sachalinensis; water extracts of Rhodiola root elicit positive effects on the human central nervous system and improve brain function. They are also thought to be beneficial to one's health, in addition to being antioxidants. The present study aims to evaluate the anti-Huntington's effect of rosiridin against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD)-like effects in rats. Materials and Methods: The acute toxicity in rats was elucidated to track the conceivable toxicities in the rats. The effectiveness of rosiridin at a dosage of 10 mg/kg was evaluated against several dose administrations of 3-NPA-induced HD-like symptoms in the rats for 22 days. At the end of the study, behavioral parameters were assessed as a hallmark for the cognitive and motor functions in the rats. Similarly, after the behavioral assessment, the animals were sacrificed to obtain a brain tissue homogenate. The prepared homogenate was utilized for the estimation of several biochemical parameters, including oxidative stress (glutathione, catalase, and malondialdehyde), brain-derived neurotrophic factor and succinate dehydrogenase activity, and the glutamate and acetylcholinesterase levels in the brain. Furthermore, inflammatory mediators linked to the occurrence of neuroinflammation in rats were evaluated in the perfused brain tissues. Results: The rosiridin-treated group exhibited a significant restoration of behavioral parameters, including in the beam-walk test, latency in falling during the hanging wire test, and percentage of memory retention during the elevated plus-maze test. Further, rosiridin modulated several biochemical parameters, including oxidative stress, pro-inflammatory activity, brain-derived neurotrophic factor, nitrite, and acetylcholinesterase as compared to disease control group that was treated with 3-NPA. Conclusions: The current study exhibits the anti-Huntington's effects of rosiridin in experimental animal models.

Rosinidin Flavonoid Ameliorates Hyperglycemia, Lipid Pathways and Proinflammatory Cytokines in Streptozotocin-Induced Diabetic Rats.

Diabetes is one of the world's most important public health issues, impacting both public health and socioeconomic advancement; moreover, current pharmacotherapy is still insufficient. The natural flavonoid rosinidin has a long history of use in pharmaceuticals and nutritional supplements, but its role in diabetes has been unknown. The current study was intended to confirm the anti-diabetic activity of rosinidin in our laboratory setting, along with its mechanism. Streptozotocin (60 mg/kg, ip) treatment used to induce type II diabetes in rats and the test medication rosinidin was then administered orally (at doses of 10 mg/kg and 20 mg/kg) for biochemical and histopathological analysis. Treatment with rosinidin reduced negative consequences of diabetes. Rosinidin exerted a protective effect on a number of characteristics, including anti-diabetic responses (lower blood glucose, higher serum insulin and improved pancreatic function) and molecular mechanisms (favorable effects on lipid profiles, total protein, albumin, liver glycogen, proinflammatory cytokine, antioxidant and oxidative stress markers, AST, ALT and urea). Furthermore, the improved pancreatic architecture observed in tissues substantiated the favourable actions of rosinidin in STZ-induced diabetic rats.

Butin Attenuates Arthritis in Complete Freund's Adjuvant-Treated Arthritic Rats: Possibly Mediated by Its Antioxidant and Anti-Inflammatory Actions.

The present research work was planned to evaluate the antioxidant and anti-inflammatory actions of butin in preventing complete Freund's adjuvant-induced arthritis in rats. Adult Wistar rats (200-240 g) were segregated equally into four groups: Group I (normal) and Group II complete Freund's adjuvant (CFA control) were administered orally with 3 ml/kg of 0.5% SCMC (vehicle); Group III and Group IV were test groups and orally administered 25 and 50 mg/kg of butin. These oral treatments were administered for a total of 21 days. In the 21-day treatment schedule, on the first day, animals from group I (normal control) were injected a single dose of normal saline (0.1 ml) intradermally into one of the hind paws, and animals from Group II to IV were injected CFA (0.1 ml) intradermally into one of the hind paws. During the treatment schedule, the volume of the hind paw and body weight were recorded at every 7 days intervals, and animals were scored for severe arthritis on days 17, 19, and 21. On the 22nd day, samples of blood were withdrawn by puncturing the retro-orbital sinus for analysis of RBC, WBC, hemoglobin, ALT, AST, ALP, PGE2, and cytokines. After blood withdrawal, animals were euthanized; the paw was separated by cutting at the ankle joint and used for analysis of oxidative stress and antioxidant parameters, as well as for the histopathological study. Administration of butin to CFA-treated animals significantly attenuated the CFA-induced inflammatory response, oxidative stress, and reversed the histopathological alteration towards normal. According to the findings, butin has anti-inflammatory and anti-arthritic properties in rats with CFA-induced arthritis.