As the world, and the United States, waits anxiously for news of when the outbreak and lockdown will end, two new plans outline requirements that will significantly impact our already suspended civil liberties.
PMID:
Pharmacology. 2018 ;102(1-2):58-66. Epub 2018 Jun 7. PMID: 29879712
Abstract Title:
Galangin Induces Apoptosis in MCF-7 Human Breast Cancer Cells Through Mitochondrial Pathway and Phosphatidylinositol 3-Kinase/Akt Inhibition.
Abstract:
AIMS: The study aimed to investigate the molecular mechanism of inhibition of proliferation and apoptosis induction by galangin against MCF-7 human breast cancer cells.METHODS: Cell Counting Kit-8 assay was used to assess cell viability and flow cytometry was used to detect cell apoptosis. The expression level of apoptosis-related proteins (cleaved-caspase-9, cleaved-caspase-8, cleaved-caspase-3, Bad, cleaved-Bid, Bcl-2, Bax, p-phosphatidylinositol 3-kinase [PI3K], and p-Akt) and cell cycle-related proteins (cyclin D3, cyclin B1, cyclin-dependent kinases CDK1, CDK2, CDK4, p21, p27, p53) were evaluated by Western blotting.RESULTS: Galangin increased the expression of Bax and decreased the expression of Bcl-2 in a concentration-dependent manner, inhibited cell viability, and induced apoptosis. Meanwhile, the expression of cleavage of caspase-9, caspase-8, caspase-3, Bid, and Bad increased significantly while the expression of p-PI3K and p-Akt proteins decreased. In addition, the protein levels of cyclin D3, cyclin B1, CDK1, CDK2, and CDK4 were downregulated while the expression levels of p21, p27, and p53 were upregulated significantly.CONCLUSION: Galangin could suppress the viability of MCF-7 cells and induce cell apoptosis via the mitochondrial pathway and PI3K/Akt inhibition as well as cell cycle arrest.
PMID:
Pharm Biol. 2018 Dec ;56(1):302-308. PMID: 29952676
Abstract Title:
Galangin, a dietary flavonoid, ameliorates hyperglycaemia and lipid abnormalities in rats with streptozotocin-induced hyperglycaemia.
Abstract:
CONTEXT: Galangin, a natural flavonoid, is found in honey and Alpinia officinarum Hance (Zingiberaceae). Galangin has antiviral, antimicrobial, antidiabetic and anticancer properties, without side effects. The effects of galangin on hyperglycaemia and lipid abnormalities are not known.OBJECTIVE: To elucidate the effectiveness of galangin on hyperglycaemia-associated complications and lipid changes in rats with streptozotocin (STZ)-induced hyperglycaemia.MATERIALS AND METHODS: Diabetes was induced in adult Wistar rats by administering 40 mg/kg of STZ. In our previous study, galangin had no toxicity at concentrations up to 320 mg/kg. Therefore three doses of galangin (4, 8 or 16 mg/kg BW) or glibenclamide (600 µg/kg BW) were administered daily to diabetic rats orally for 45 days.RESULTS: Diabetic rats showed a significant (p
PMID:
Mol Cell Biochem. 2019 Jan ;451(1-2):145-153. Epub 2018 Jul 11. PMID: 29995265
Abstract Title:
Anti-neuroinflammatory effects of galangin in LPS-stimulated BV-2 microglia through regulation of IL-1β production and the NF-κB signaling pathways.
Abstract:
Neuroinflammation resulting from microglial activation is involved in the pathogenesis of neurodegenerative diseases, including Parkinson's diseases. Microglial activation plays an important role in neuroinflammation and contributes to several neurological disorders. Hence, inhibition of both microglial activation and the generation of pro-inflammatory cytokines may lead to an effective treatment for neurodegenerative diseases. In the present study, the anti-neuroinflammatory effects of galangin were investigated in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Galangin significantly decreased the generation of nitric oxide, interleukin-1β, and inducible nitric oxide synthase in LPS-stimulated BV-2 microglial cells. In addition, galangin inhibited the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase 1/2. Furthermore, it was observed that activation of both IκB-α and nuclear factor kappa B(NF-κB) was significantly increased following LPS stimulation, and this effect was suppressed by galangin treatment. In conclusion, galangin displayed an anti-neuroinflammatory activity in LPS-stimulated BV-2 microglial cells. Galangin inhibited LPS-induced neuroinflammation via the MAPK and NF-κB signaling pathways and might act as a natural therapeutic agent for the treatment of various neuroinflammatory conditions.
PMID:
J BUON. 2018 May-Jun;23(3):795-799. PMID: 30003754
Abstract Title:
Galangin induced antitumor effects in human kidney tumor cells mediated via mitochondrial mediated apoptosis, inhibition of cell migration and invasion and targeting PI3K/ AKT/mTOR signalling pathway.
Abstract:
PURPOSE: Galangin is an important flavonoid that has been reported to be of immense pharmacological importance. It has been shown to have a number of bioactivities which range from anticancer to antimicrobial. In this study the effects of Galangin were studied on the proliferation of the A498 kidney cancer cells.METHODS: The antiproliferative effects were tested by MTT assay. Apoptosis was checked by subjecting the A498 cell to DAPI and annexin V/PI double staining. The effect on the cell migration and invasion was assessed by Boyden chamber assays. The expression of the apoptosis-related proteins was examined by western blot analysis.RESULTS: Galangin inhibited the proliferation of the kidney cancer A498 cells. The IC50 of Galangin against the A498 cancer cells was 15μM. The anticancer effects of Galangin were due to induction of apoptosis in the A498 cancer cells as indicated by DAPI and annexin V/PI staining. Furthermore, Galangin could increase the expression of Bax, Cyt-c and decrease the expression of Bcl-2. Galangin could also inhibit the migration and invasion of the kidney cancer cells and also suppress the expression of some of the important proteins of the PI3K/AKT/mTOR signalling pathway.CONCLUSION: In conclusion, Galangin could prove a useful new molecule in the treatment of kidney carcinoma.
PMID:
Food Chem. 2019 Jan 15 ;271:70-79. Epub 2018 Jul 24. PMID: 30236734
Abstract Title:
Galangin inhibitsα-glucosidase activity and formation of non-enzymatic glycation products.
Abstract:
Inhibition ofα-glucosidase and non-enzymatic glycation is considered as an effective approach to treat type 2 diabetes. Herein, multispectroscopic techniques and molecular docking analysis were used to investigate the inhibition of galangin on α-glucosidase and non-enzymatic glycation. Galangin showed a reversible inhibition on α-glucosidase activity in a mixed-type manner through a monophasic kinetic process, and induced the fluorescence quenching and conformational changes of α-glucosidase by forming α-glucosidase-galgangin complex. Molecular docking revealed that galangin primarily interacted withthe amino acid residues within the active site of α-glucosidase, which may prevent the entrance of substrate resulting in a decrease in catalytic efficiency of α-glucosidase. Moreover, galangin moderately inhibited the formation of intermediates of non-enzymatic glycation, fructosamine and α-dicarbonyl compounds and strongly inhibited the formation of advanced glycation end products.
PMID:
Cell Physiol Biochem. 2018 ;51(3):1354-1363. Epub 2018 Nov 27. PMID: 30481779
Abstract Title:
Galangin Alleviates Liver Ischemia-Reperfusion Injury in a Rat Model by Mediating the PI3K/AKT Pathway.
Abstract:
BACKGROUND/AIMS: Liver ischemia-reperfusion (I/R) injury is a pathological process that often occurs during liver and trauma surgery. There are numerous causes of liver I/R injury, but the mechanism is unknown. Galangin (GA) is a flavonoid, a polyphenolic compound widely distributed in medicinal herbs that has anti-inflammatory, antioxidant, and antitumor activity. This study evaluated the protective effect of GA on hepatic I/R injury.METHODS: An I/R model was created in male Wistar rats by clamping the hepatoportal vein, hepatic artery and hepatic duct for 30 min followed by reperfusion for 2 h. A hypoxia/restoration (H/R) model was established in buffalo rat liver (BRL) cells by hypoxia for 4 h followed by normoxic conditions for 10 h. The extent of liver injury was assayed by serum ALT/AST, hepatic histology, and MPO activity. Oxidative stress was assayed by serum superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA). Expression of apoptosis-related proteins in BRL cells was assayed in western blots. Expression of AKT and p-AKT proteins in vivo and vitro were assayed in western blots.RESULTS: GA significantly decreased ALT/AST expression, reversed changes in oxidative stress markers induced by I/R, and mediated caspase-3 activity expression of apoptosis-related proteins in vivo and in vitro. Methylthiazol tetrazolium (MTT) assay, flow cytometry, and Hoechst 33258 staining confirmed that GA inhibited apoptosis of BRL cells. GA also increased the expression of phosphorylated AKT after H/R.CONCLUSION: GA reduced liver I/R injury both in vivo and vitro and inhibited BRL cell apoptosis. PI3K/AKT signaling have been involved. GA may protect against liver I/R and be a potential therapeutic candidate.
PMID:
Biomed Pharmacother. 2019 Jan ;109:2054-2061. Epub 2018 Nov 26. PMID: 30551461
Abstract Title:
Chemopreventive mechanisms of galangin against hepatocellular carcinoma: A review.
Abstract:
Hepatocellular carcinoma (HCC) is one of the most common cancers and has a high mortality rate in less developed countries, especially in China. Galangin (GA), one of the most important and naturally active flavonoids, extracted primarily from the root of Alpinia officinarum Hance, has been demonstrated to be effective in the treatment of HCC. It is a substance with defensive actions and a broad range of biological properties, including inhibitory effects on bacteria, fungi, viruses, the control of hypertension and diabetes, and chemoprevention of several cancers. Experiments have shown that GA prevents HCC through multiple anti-cancer mechanisms, anti-genotoxic activity against environmental and dietary carcinogens; anti-proliferative effects through reversal of the Warburg effect in HCC; arrest of the cell cycle in the G0/G1 phase; induction of apoptosis via stimulation of reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and the mitochondrial-dependent apoptosis pathway; induction of autophagy; and inhibition of angiogenesis, metastasis, and multidrug resistance (MDR). In addition, synergistic effects with other chemotherapy drugs have been demonstrated. Therefore, this review is focused on the anti-HCC mechanisms of GA.
PMID:
Neuroscience. 2019 08 10 ;413:154-168. Epub 2019 Jun 11. PMID: 31200106
Abstract Title:
Galangin Prevents Increased Susceptibility to Pentylenetetrazol-Stimulated Seizures by Prostaglandin E2.
Abstract:
Epilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators, such as prostaglandin E(PGE), during seizures. The purpose of this study was to investigate whether PGEincreases susceptibility to pentylenetetrazol-induced (PTZ) seizures. Subsequently, we evaluated if the flavonoid isolated from the plant Piper aleyreanum (galangin) presented any anticonvulsive effects. Our results demonstrated that the group treated with PGEincreased susceptibility to PTZ and caused myoclonic and generalized seizures, which increased seizure duration and electroencephalographic wave amplitudes. Furthermore, treatment with PGEand PTZ increased IBA-1 (microglial marker), GFAP (astrocytic marker), 4-HNE (lipid peroxidation marker), VCAM-1 (vascular cell adhesion molecule 1), and p-PKAIIα (phosphorylated cAMP-dependent protein kinase) immunocontent. Indeed, galangin prevented behavioral and electroencephalographic seizures, reactive species production, decreased microglial and astrocytic immunocontent, as well as decreased VCAM-1 immunocontent and p-PKA/PKA ratio induced by PGE/PTZ. Therefore, this study suggests galangin may have an antagonizing role on PGE-induced effects, reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGEand PTZ. However, further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms.
PMID:
Biomolecules. 2019 08 5 ;9(8). Epub 2019 Aug 5. PMID: 31387329
Abstract Title:
Galangin Activates Nrf2 Signaling and Attenuates Oxidative Damage, Inflammation, and Apoptosis in a Rat Model of Cyclophosphamide-Induced Hepatotoxicity.
Abstract:
Cyclophosphamide (CP) is a widely used chemotherapeutic agent; however, its clinical application is limited because of its multi-organ toxicity. Galangin (Gal) is a bioactive flavonoid with promising biological activities. This study investigated the hepatoprotective effect of Gal in CP-induced rats. Rats received Gal (15, 30 and 60 mg/kg/day) for 15 days followed by a single dose of CP at day 16. Cyclophosphamide triggered liver injury characterized by elevated serum transaminases, alkaline phosphatase (ALP) and lactate dehydrogenase (LDH), and histopathological manifestations. Increased hepatic reactive oxygen species, malondialdehyde, nitric oxide, and oxidative DNA damage along with declined glutathione and antioxidant enzymes were demonstrated in CP-administered rats. CP provoked hepatic nuclear factor-kappaB (NF-κB) phosphorylation and increased mRNA abundance of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) both expression and serum levels. Gal prevented CP-induced liver injury, boosted antioxidants and suppressed oxidative stress, DNA damage, NF-κB phosphorylation and pro-inflammatory mediators. Gal diminished Bax and caspase-3, and increased B-cell lymphoma-2 (Bcl-2) in liver of CP-administered rats. In addition, Gal increased peroxisome proliferator-activated receptor gamma (PPARγ) expression and activated hepatic nuclear factor erythroid 2-related factor 2 (Nrf2) signaling showed by the increase in Nrf2, NAD(P)H: quinone acceptor oxidoreductase-1 (NQO-1) and heme oxygenase 1 (HO-1) in CP-administered rats. These findings suggest that Gal prevents CP hepatotoxicity through activation of Nrf2/HO-1 signaling and attenuation of oxidative damage, inflammation and cell death. Therefore, Gal might represent a promising adjuvant therapy to prevent hepatotoxicity in patients on CP treatment.
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