Catalpol

1 Euphrasia sp. 2 Globularia sp. 3 Picrorhiza sp. 4 Pinguicula sp. 5 Plantago sp. 6 Rehmannia sp. 7 Scrophularia sp. 8 Verbascum sp. 9 Veronica sp.

Catalpol, an iridoid glycoside, has neuroprotective, anti-inflammatory, and anti-hepatitis virus effects. IC50 Value: Target: neuroprotective, anti-inflammatory, and anti-hepatitis virus natural product. In vitro: Catalpol could be encapsulated into composite nanofibers and induce differentiation of hASCs into neural-like cells, which might offer new avenues in nerve regeneration [1]. In vivo: The pharmacokinetics of catalpol in normal and doxorubicin-induced chronic kidney disease rats after oral administration of Rehmannia glutinosa extract was determined, and the extraction recoverie of catalpol was higher than 68.24% [2]. The protective effect of catalpol on renal IRI mice through suppressing phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt)-endothelial nitric oxide synthase (eNOS) and against inflammation, and the possible underlying mechanism [3].

References:
[1]. Zhao M, et al.Comparative pharmacokinetics of catalpol and acteoside in normal and chronic kidney disease rats after oral administration of Rehmannia glutinosa extract. Biomed Chromatogr. 2015 May 29. [2]. Guo JH, et al.Potential Neurogenesis of Human Adipose-Derived Stem Cells on Electrospun Catalpol-Loaded Composite Nanofibrous Scaffolds. Ann Biomed Eng. 2015 Mar 31. [3]. Zhu J,Catalpol protects mice against renal ischemia/reperfusion injury via suppressing PI3K/Akt-eNOS signaling and inflammation. Int J Clin Exp Med. 2015 Feb 15;8(2):2038-44. [4]. Xu Z, et al.Mitochondrial fusion/fission process involved in the improvement of catalpol on high glucose-induced hepatic mitochondrial dysfunction. Acta Biochim Biophys Sin (Shanghai). 2015 Jul 2.

Catalpol inhibits apoptosis in hydrogen peroxide-induced cardiac myocytes through a mitochondrial-dependent caspase pathway.[Pubmed:27166426]

Biosci Rep. 2016 Jun 30;36(3). pii: BSR20160132.

Catalpol, an iridoid glucoside, has been reported to inhibit apoptosis of neuron and endothelial cells. In the present study, we investigated the mechanism of Catalpol-mediated cardioprotection. The rat embryonic ventricular myocardial cell line (H9c2) cells were first incubated with Catalpol, and then exposed to hydrogen peroxide (H2O2). The concentration of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were all determined by using commercially available kits. Apoptotic cells were assessed by Hoechst 33258 and Annexin V-fluorescein isothiocyanate binding assay. Synthesis of Bcl-2, Bax, cytochrome c and caspase-3 were analysed by real-time semiquantitative reverse transcription-PCR and Western blotting. We observed that apoptosis in H9c2 was associated with increased Bax, cytochrome c, caspase-3, decreased Bcl-2 activity after 24 h of H2O2 exposure. Catalpol pretreatment afforded a marked protection against the above H2O2-mediated cytotoxicity and apoptosis in H9c2 cells. Moreover, the Catalpol pretreatment led to a great reduction in H2O2-induced MDA release and increased SOD. These findings indicated for the first time that pretreatment of H9c2 cells with Catalpol can be against H2O2-induced apoptosis, and the protective effect of Catalpol involves the mitochondrial-dependent caspase pathway and is associated with increased Bcl-2 and decreased Bax expression.

Catalpol protects primary cultured astrocytes from in vitro ischemia-induced damage.[Pubmed:18337048]

Int J Dev Neurosci. 2008 May-Jun;26(3-4):309-17.

Catalpol, an iridoid glycoside abundant in the roots of Rehmannia glutinosa, has been previously found to prevent the loss of CA1 hippocampal neurons and to reduce working errors in gerbils after ischemia-reperfusion injury. In the present study, we investigated the effects of Catalpol on astrocytes in an ischemic model to further characterize its neuroprotective mechanisms. Primary cultured astrocytes exposed to oxygen-glucose deprivation (OGD) followed by reperfusion (adding back oxygen and glucose, OGD-R), were used as an in vitro ischemic model. Treatment of the astrocytes with Catalpol during ischemia-reperfusion increased astrocyte survival significantly in a concentration-dependent manner, as demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, lactate dehydrogenase (LDH) release and morphological observation. In addition, Catalpol prevented the decrease in mitochondrial membrane potential, inhibited the formation of reactive oxygen species (ROS) and the production of nitric oxide (NO), decreased the level of lipid peroxide and the activity of inducible nitric oxide synthase (iNOS), and elevated the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and the content of glutathione (GSH). Our results suggest that Catalpol exerts the most significant cytoprotective effect on astrocytes by suppressing the production of free radicals and elevating antioxidant capacity.

Catalpol promotes oligodendrocyte survival and oligodendrocyte progenitor differentiation via the Akt signaling pathway in rats with chronic cerebral hypoperfusion.[Pubmed:24632336]

Brain Res. 2014 Apr 29;1560:27-35.

Chronic cerebral hypoperfusion is thought to induce white matter lesions (WMLs), which contribute to cognitive impairment. Although inflammation and oligodendrocyte apoptosis are believed to be involved in the pathogenesis of WMLs, effective therapies have not been identified yet. This study investigated whether Catalpol, an iridoid glycoside, can alleviate WMLs by promoting oligodendrocyte survival and oligodendrocyte progenitor differentiation via the Akt signaling pathway in rats with chronic cerebral hypoperfusion. A rat model of chronic cerebral hypoperfusion was created through permanent occlusion of bilateral common carotid arteries. Catalpol (5mg/kg) or saline was intraperitoneally administered daily for 10 days following the operation. On the 30th day after surgery, inflammation, oligodendrocyte apoptosis, and myelin damage in the ischemic white matter were more severe and evident than in the sham control group. Treatment with Catalpol significantly suppressed white matter inflammation and attenuated oligodendrocyte apoptosis and myelin damage. The expression of phosphorylated Akt (p-Akt) and the number of mature oligodendrocytes were also markedly increased by Catalpol treatment, and these effects were reversed by the PI3K inhibitor LY294002. In conclusion, Catalpol attenuates hypoperfusion-induced WMLs by promoting oligodendrocyte survival and oligodendrocyte progenitor differentiation through the Akt signaling pathway. Our results suggest that Catalpol may be a candidate for treating cerebrovascular WMLs.

Catalpol regulates cholinergic nerve system function through effect on choline acetyl-transferase not M receptor affinity.[Pubmed:25661372]

Biomed Pharmacother. 2015 Feb;69:291-6.

OBJECTIVE: To explore the effect of Catalpol on choline acetyl-transferase and M receptor affinity in a PC12 cell model and a rat model induced by beta-amyloid 25-35 (Abeta25-35). METHODS: In PC12 cells, Catalpol (10mumol/l, 100mumol/) or saline was retained in the medium and Abeta25-35 (final concentration 20mumol/l) was added. Choline acetyl-transferase (ChAT) expression was determined by immunocytochemistry, ChAT activity measured by radioenzymatic assay, and M receptor (muscarinic receptor) affinity determined by (3)H-QNB binding test. In Wistar rats, Abeta25-35 was injected intracerebroventricularly to establish AD model. After injection of Abeta25-35, the rats were injected Catalpol at 5 and 10mg/kgd(-1) intraperitoneally for the next 7 days, and saline for the control rats. ChAT expression, ChAT activity and M receptor affinity were tested. Cells and rats all were divided into four groups: Group A (control), Group B (model), Group C (Catalpol low dose), and Group D (Catalpol high dose). RESULTS: Compared with control, both PC12 cell and rat AD models showed decreased expression and activity of ChAT (p<0.01), but M receptor affinity remained the same (p>0.05). Compared with model group, treatment of Catalpol increased expression and activity of ChAT of PC12 cell and rat AD model induced by Abeta25-35, p<0.05 or p<0.01 respectively. But there was no difference of M receptor affinity among the four groups (p>0.05). M receptor affinity remained the same as concentration of Catalpol increased gradually in atropine competition experiments (p>0.05). CONCLUSIONS: Catalpol could regulate the cholinergic nerve system function from its effect on ChAT and may have beneficial effect for treatment of AD, but had no effect on M receptor affinity.

Catalpol provides protective effects against cerebral ischaemia/reperfusion injury in gerbils.[Pubmed:24720795]

J Pharm Pharmacol. 2014 Sep;66(9):1265-70.

OBJECTIVES: To investigate the protective effect of Catalpol on cerebral ischaemia/reperfusion (CI/R) injury in gerbils and further explore the underlying mechanism. METHODS: A gerbil model of CI/R was prepared by bilateral common carotid occlusion for 10 min followed by 6 h reperfusion. Catalpol (5, 10 or 20 mg/kg per day) was injected intraperitoneally for 3 days before the carotid occlusion. Stroke index was measured during the reperfusion. The contents of endogenous neuropeptides, endothelin-1 (ET-1) and calcitonin gene-related peptide in plasma were evaluated by radioimmunoassay. Superoxide dismutase (SOD) and malondialdehyde (MDA) in brain tissue homogenate were also examined. KEY FINDINGS: The results showed that Catalpol significantly improved the stroke index compared with CI/R control group (P < 0.05 or P < 0.01). Catalpol significantly increased the activity of SOD at the doses of 10 and 20 mg/kg (P Catalpol pretreatment on CI/R injury may be attributed to reduction of free radicals and inhibition of lipid peroxidation and ET-1 production.

Protective effect of catalpol on lipopolysaccharide-induced acute lung injury in mice.[Pubmed:25063711]

Int Immunopharmacol. 2014 Dec;23(2):400-6.

Catalpol, an iridiod glucoside isolated from Rehmannia glutinosa, has been reported to have anti-inflammatory properties. Although anti-inflammatory activity of Catalpol already reported, its involvement in lung protection has not been reported. Thus, we investigated the role of Catalpol on lipopolysaccharide (LPS)-induced acute lung injury in this study. Mice acute lung injury model was induced by intranasal instillation of LPS. Catalpol was administrated 1h prior to or after LPS exposure. The severity of pulmonary injury was evaluated 12h after LPS administration. The results showed that Catalpol inhibited lung W/D ratio, myeloperoxidase activity of lung samples, the amounts of inflammatory cells and TNF-alpha, IL-6, IL-4 and IL-1beta in BALF induced by LPS. The production of IL-10 in BALF was up-regulated by Catalpol. In vitro, Catalpol inhibited TNF-alpha, IL-6, IL-4 and IL-1beta production and up-regulated IL-10 expression in LPS-stimulated alveolar macrophages. Moreover, western blot analysis showed that the activation of NF-kappaB and MAPK signaling pathways was inhibited by Catalpol. Furthermore, Catalpol was found to inhibit TLR4 expression induced by LPS. In conclusion, Catalpol potently protected against LPS-induced ALI. The protective effect may attribute to the inhibition of TLR4-mediated NF-kappaB and MAPK signaling pathways.

Catalpol protects mice against renal ischemia/reperfusion injury via suppressing PI3K/Akt-eNOS signaling and inflammation.[Pubmed:25932134]

Int J Clin Exp Med. 2015 Feb 15;8(2):2038-44. eCollection 2015.

Renal ischemia/reperfusion-injury (IRI) is a common disease in clinic, which is also the most common cause of acute kidney failure. Previous investigations has illustrated that Catalpol has neuroprotective, anti-inflammatory, and anti-hepatitis virus effects. This study was designed to investigate the protective effect of Catalpol on renal IRI mice through suppressing phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt)-endothelial nitric oxide synthase (eNOS) and against inflammation, and the possible underlying mechanism. Firstly, we used renal IRI model to analyze blood urea nitrogen and serum creatinine levels in renal IRI mice. Next, real-time PCR and western blotting were used to detect the expression of KIM-1 and the expression of PI3K, Akt and eNOS levels in renal IRI, respectively. In addition, activities of tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and interleukin-10 (IL-10) in renal IRI mice were measured with respective TNF-alpha, IL-1beta, IL-6 and IL-10 ELISA kits. Our results showed that Catalpol clearly reduced blood urea nitrogen, serum creatinine levels and the expression of KIM-1 in renal IRI mice. Meanwhile, we found that Catalpol markedly reduced the expression of PI3K, Akt and eNOS levels in renal IRI group. Suppressing of the PI3K/Akt-eNOS and the TNF-alpha, IL-1beta, IL-6 and IL-10 activities was involved in the protective effect of Catalpol on renal IRI. Collectively, Catalpol protected renal IRI via inhibiting PI3K/Akt-eNOS signaling and inflammatory responses.

Catalpol, an iridoid glycoside, has neuroprotective, anti-inflammatory, and anti-hepatitis virus effects.

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