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Carthamus tinctorius may be used as an alternative therapeutic agent while treating patients with anxiety and depressive disorders.

PMID:

Pak J Pharm Sci. 2015 May ;28(3):991-5. PMID: 26004733

Abstract Title:

Short communication-Evaluation of antianxiety and antidepressant properties of Carthamus tinctorius L. (Safflower) petal extract.

Abstract:

Nowadays anxiety and depression are most commonly encountered diseases. They are not only difficult to diagnose but even difficult to treat since both are sometimes seen together or one predisposes the other. Apart from this side effect profile of these drugs is also high; hence there is immense scope for the herbal drugs to treat these disorders. Present study was therefore performed to evaluate the antianxiety and antidepressant effect of Carthamus tinctorius petal extract. 28 white albino rats bred in the animal house of Department of Pharmacology, University of Karachi weighing 180-220gm were randomly divided into four groups (n=7/group) to assess behavioral effects. The anxiolytic and antidepressant effects of Carthamus tinctorius petal extract were evaluated using elevated plus maize and forced swim test respectively at100 and 200mg/kg. These effects were compared with standard drugs Diazepam (anxiolytic) 2mg/kg and Nortriptyline (antidepressant) 12.5mg/kg. Results show that CT produced highly significant anxiolytic and anti-depressant effects at both doses as compared to control, similar to standard anxiolytic and antidepressant drugs diazepam and nortriptyline. It increased the latency of first entry to closed arms and the time spent in open arms very significantly at both doses while entries to open arm were increased significantly at 100mg/kg and very significantly at 200mg/kg in EPM test and increased the immobility time very significantly in FST. Hence it can be concluded that CT may be used as an alternative therapeutic agent while treating patients with anxiety and depressive disorders.

Protective effect of Salvia miltiorrhiza and Carthamus tinctorius extract against lipopolysaccharide-induced liver injury.

PMID:

World J Gastroenterol. 2015 Aug 14 ;21(30):9079-92. PMID: 26290634

Abstract Title:

Protective effect of Salvia miltiorrhiza and Carthamus tinctorius extract against lipopolysaccharide-induced liver injury.

Abstract:

AIM: To investigate the hepatoprotective effects and mechanisms of an extract of Salvia miltiorrhiza and Carthamus tinctorius in vivo.METHODS: C57BL/6J mice were randomly assigned to five groups and intraperitoneally administered 0.9% saline, Salvia miltiorrhiza and Carthamus tinctorius extract [Danhong injection (DHI), 0.75 and 3 g/kg mixed extract] or reduced glutathione for injection (RGI, 300 mg/kg) for 30 min before exposure to lipopolysaccharide (LPS, 16 mg/kg). After intraperitoneal LPS stimulation for 90 min or 6 h, the mice were sacrificed by ether anaesthesia, and serum and liver samples were collected. Histological analysis (H&E) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling (TUNEL) staining were performed. Alanine transferase (ALT), aspartate transaminase (AST), total bilirubin (TBil), glutathione-S-transferase (GST), malondialdehyde (MDA), tumour necrosis factor (TNF)-α, interleukin (IL)-6, and caspase-3 levels were measured. Bax, Bcl-2, P-IκBα, IκBα, P-NF-κB p65, and NF-κB p65 protein levels were determined by Western blot. TNF-α, IL-6, caspase-3, Bax and Bcl-2 mRNA expression was measured by real-time reverse transcription-polymerase chain reaction (RT-PCR).RESULTS: Hematoxylin-eosin staining and TUNEL results suggested that DHI (3 g/kg) treatment alleviated inflammatory and apoptotic (P

Ginsenoside Rh2 exerts anti-metastasis activity in hypoxic tumor microenvironment in lung adenocarcinoma cells via mir-491.

PMID:

Anticancer Agents Med Chem. 2019 Jul 4. Epub 2019 Jul 4. PMID: 31272362

Abstract Title:

Ginsenoside Rh2 Inhibits Migration of Lung Cancer Cells Under Hypoxia via mir-491.

Abstract:

BACKGROUND: Ginsenoside Rh2 (Rh2), which is extracted form ginseng, exerts antitumor activity. Here we would like to study the role of Rh2 on hypoxia-induced migration in lung adenocarcinoma.METHODS: Lung adenocarcinoma A549 and H1299 cells were cultured in 1% O2 condition to mimic the hypoxic tumor microenvironment. The migrations of cancer cells were measured by transwell assay and scratch assay.RESULTS: Rh2 could inhibit hypoxia -induced A549 and H1299 cell migration via increase of mir-491expression. Further, mir-491 antisense oligonucleotide could repress hypoxia-induced migration and the expression of matrix metalloproteinase (MMP)-9 expression in Rh2-treated A549 cells.CONCLUSION: These findings suggest that Rh2 exerts anti-metastasis activity in hypoxic tumor microenvironment in lung adenocarcinoma cells via mir-491.

This data clarifies the potential therapeutic significance of ginsenoside Rg1 for neuroprotective intervention strategies of diabetic retinopathy.

PMID:

J Agric Food Chem. 2019 Jul 31 ;67(30):8348-8360. Epub 2019 Jul 19. PMID: 31304751

Abstract Title:

Neuroprotective Effects of Ginsenoside Rg1 against Hyperphosphorylated Tau-Induced Diabetic Retinal Neurodegeneration via Activation of IRS-1/Akt/GSK3β Signaling.

Abstract:

We have recently demonstrated that tau hyperphosphorylation causes diabetic synaptic neurodegeneration of retinal ganglion cells (RGCs), which might be the earliest affair during the pathogenesis of diabetic retinopathy (DR). Thus, there is a pressing need to seek therapeutic agents possessing neuroprotective effects against tau hyperphosphorylation in RGCs for arresting the progression of DR. Here, using a well-characterized diabetes model of/mouse, we discovered that topical ocular application of 10 mg/kg/day of ginsenoside Rg1 (GRg1), one of the major active ingredients extracted fromand, ameliorated hyperphosphorylated tau-triggered RGCs synaptic neurodegeneration in diabetic mice. The neuroprotective effects of GRg1 on diabetic retinae were abrogated when retinal IRS-1 or Akt was suppressed by intravitreal injection with si-or topically coadministered with a specific inhibitor of Akt, respectively. However, selective repression of retinal GSK3β by intravitreal administration of si-rescued the neuroprotective properties of GRg1 when Akt was inactivated. Therefore, the present study showed for the first time that GRg1 can prevent hyperphosphorylated tau-induced synaptic neurodegeneration of RGCs via activation of IRS-1/Akt/GSK3β signaling in the early phase of DR. Moreover, our data clarify the potential therapeutic significance of GRg1 for neuroprotective intervention strategies of DR.

Ginsenoside Rb1 inhibits proliferation and promotes apoptosis by regulating HMGB1 in uterine fibroid cells.

PMID:

Artif Cells Nanomed Biotechnol. 2019 Dec ;47(1):2967-2971. PMID: 31313594

Abstract Title:

Ginsenoside Rb1 inhibits proliferation and promotes apoptosis by regulating HMGB1 in uterine fibroid cells.

Abstract:

To study the effects of ginsenoside Rb1 and the molecular mechanisms on proliferation and apoptosis of uterine fibroid cells, Rb1 + pc DNA3.1, Rb1 + pc DNA3.1-HMGB1, si-NC or si-HMGB1 was transfected into uterine fibroid cells by liposome method; the inhibitory rate and proliferation of human uterine fibroid cells were detected by MTT assay; apoptosis of uterine fibroid cells was detected by flow cytometry assay; HMGB1 protein expression in uterine fibroid cells was detected by Western blot assay. Compared with untreated uterine fibroid cells, the inhibitory and apoptosis rate of uterine fibroid cells treated with Rb1 were significantly up-regulated, while the expression level of HMGB1 was significantly down-regulated (

Ginsenoside compound K inhibits nuclear factor-kappa B by targeting Annexin A2.

PMID:

J Ginseng Res. 2019 Jul ;43(3):452-459. Epub 2018 Apr 21. PMID: 31308817

Abstract Title:

Ginsenoside compound K inhibits nuclear factor-kappa B by targeting Annexin A2.

Abstract:

Background: Ginsenoside compound K(C-K), a major metabolite of ginsenoside, exhibits anticancer activity in various cancer cells and animal models. A cell signaling study has shown that C-K inhibited nuclear factor-kappa B (NF-κB) pathway in human astroglial cells and liver cancer cells. However, the molecular targets of C-K and the initiating events were not elucidated.Methods: Interaction between C-K and Annexin A2 was determined by molecular docking and thermal shift assay. HepG2 cells were treated with C-K, followed by a luciferase reporter assay for NF-кB, immunofluorescence imaging for the subcellular localization of Annexin A2 and NF-кB p50 subunit, coimmunoprecipitation of Annexin A2 and NF-кB p50 subunit, and both cell viability assay and plate clone formation assay to determine the cell viability.Results: Both molecular docking and thermal shift assay positively confirmed the interaction between Annexin A2 and C-K. This interaction prevented the interaction between Annexin A2 and NF-кB p50 subunit and their nuclear colocalization, which attenuated the activation of NF-кB and the expression of its downstream genes, followed by the activation of caspase 9 and 3. In addition, the overexpression of Annexin A2-K320A, a C-K binding-deficient mutant of Annexin A2, rendered cells toresist C-K treatment, indicating that C-K exerts its cytotoxic activity mainly by targeting Annexin A2.Conclusion: This study for the first time revealed a cellular target of C-K and the molecular mechanism for its anticancer activity.

Ginsenoside Rb1 may serve as a potential candidate for the treatment of Parkinson’s disease.

PMID:

Aging (Albany NY). 2019 Jul 17 ;11(14):5008-5034. PMID: 31314744

Abstract Title:

Ginsenoside Rb1 regulates prefrontal cortical GABAergic transmission in MPTP-treated mice.

Abstract:

Parkinson's disease (PD) is a common neurodegenerative disease, featured by motor deficits and non-motor symptoms such as cognitive impairment, and malfunction of gamma-aminobutyric acid (GABA) mediated inhibitory transmission plays an important role in PD pathogenesis. The ginsenoside Rb1 molecule, a major constituent of the extract from the Ginseng root, has been demonstrated to ameliorate motor deficits and prevent dopaminergic neuron death in PD. However, whether Rb1 can regulate GABAergic transmission in PD-associated deficits and its underlying mechanisms are still unclear. In this study, we explored the effects of Rb1 on the GABAergic synaptic transmission in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. We demonstrated that Rb1 can bind with GABARα1 and increase its expression in the SH-SY5Y cells and in the prefrontal cortex (PFC) of MPTP modeland. Furthermore, Rb1 can promote prefrontal cortical GABA level and GABAergic transmission in MPTP-treated mice. We also revealed that Rb1 may suppress presynaptic GABAR1 to enhance GABA release and GABAreceptor-mediated inhibitory transmission. In addition, Rb1 attenuated MPTP-induced dysfunctional gait dynamic and cognitive impairment, and this neuroprotective mechanism possibly involved regulating prefrontal cortical GABAergic transmission. Thus, Rb1 may serve as a potential drug candidate for the treatment of PD.

Ginsenoside Rb1 inhibits vascular calcification as a selective androgen receptor modulator.

PMID:

Eur J Pharmacol. 2019 Sep 15 ;859:172546. Epub 2019 Jul 15. PMID: 31319068

Abstract Title:

Ginsenoside Rb1 inhibits vascular calcification as a selective androgen receptor modulator.

Abstract:

Ginsenoside Rb1 (Rb1), a major component of ginseng, has a steroidal chemical structure, implying that it exerts sex hormone-like actions. Recent studies have been suggested cardioprotective actions of Rb1. However, the actions of Rb1 in vascular calcification, one of the significant pathological features associated with aging and atherosclerosis, have not been examined. In the present study, we examined the effects of Rb1 on vascular calcification, focusing on its androgen-like actions. Using inorganic phosphate (Pi)-induced calcification of vascular smooth muscle cells (VSMC), we found that Rb1, like testosterone, significantly inhibited calcium deposition in a concentration-dependent manner. Further, this inhibition of Rb1 was abolished by bicalutamide, an androgen receptor antagonist, but not by MPP or PHTPP, estrogen receptorα or β antagonists. Rb1 significantly inhibited apoptosis, one of the regulatory mechanisms of calcification, and restored growth arrest-specific gene 6 (Gas6) expression that was suppressed by Pi. Moreover, Rb1 transactivated Gas6, and proximal androgen-responsive element (ARE) of the promoter region was found to be crucial for Gas6 transactivation. In contrast, in a human prostate cancer cell line, testosterone-induced ARE activity was abrogated by Rb1. This antagonistic effect was also confirmed by the transrepression and downregulation of prostate-specific antigen in the presence of testosterone and Rb1 together. Thus, these findings provide a novel mechanistic insight into the vasculoprotective actions of Rb1 as a selective androgen receptor modulator, i.e., inhibitory effects on VSMC calcification through androgen receptor-mediated Gas6 transactivation and antagonistic effects inprostate cancer cells.

Ginsenoside Re could be a potential therapeutic approach for the treatment of Alzheimer’s disease.

PMID:

Molecules. 2019 Jul 24 ;24(15). Epub 2019 Jul 24. PMID: 31344860

Abstract Title:

Ginsenoside Re Inhibits ROS/ASK-1 Dependent Mitochondrial Apoptosis Pathway and Activation of Nrf2-Antioxidant Response in Beta-Amyloid-Challenged SH-SY5Y Cells.

Abstract:

Accumulation of amyloid-β (Aβ), which results in the formation of senile plaques that cause oxidative damage and neuronal cell death, has been accepted as the major pathological mechanism of Alzheimer's disease (AD). Hence, inhibition of Aβ-induced oxidative damage and neuronal cell apoptosis represents the effective strategies in combating AD. Ginsenoside Re (Re) has pharmacological effects against Aβ-induced neurotoxicity. However, its molecular mechanism remains elusive. The present study evaluated the effect of Re against Aβ-induced cytotoxicity and apoptosis in SH-SY5Y cells, and investigated the underlyingmechanism. We demonstrate that Re inhibits the Aβ-triggered mitochondrial apoptotic pathway, as indicated by maintenance of mitochondrial functional, elevated Bcl-2/Bax ratio, reduced cytochrome c release, and inactivation of caspase-3/9. Re attenuated Aβ-evoked reactive oxygen species (ROS) production, apoptosis signal-regulating kinase 1 (ASK1) phosphorylation, and JNK activation. ROS-scavenging abrogated the ability of Re to alter ASK-1 activation. Simultaneously, inhibition of JNK abolished Re-induced Bax downregulation in Aβ-challenged SH-SY5Y cells. In addition, Re enhanced activation of the nuclear factor-E2-related factor 2 (Nrf2) in Aβ-induced SH-SY5Y cells. Knockdown of Nrf2 by small interfering RNA targeting Nrf2 abolished the protective effect of Re. Our findings indicate that Re could be a potential therapeutic approach for the treatment of AD.