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Autophagy dysfunctions are involved in the pathogenesis of Parkinson’s disease (PD). In the present study, we aimed to evaluate the involvement of G protein-coupled estrogen receptor (GPER) in the inhibitory effect of insulin-like growth factor-1 (IGF-1) against excessive autophagy in PD animal and cellular models. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment significantly induced mouse movement disorder and decreased the protein level of tyrosine hydroxylase (TH) in the substantia nigra (SN) and dopamine (DA) content in striatum. Along with the dopamine neuron injury, we observed significant upregulations of microtubule-associated light chain-3 II (LC3-II) and α-synuclein as well as a downregulation of P62 in MPTP-treated mice. These changes could be restored by IGF-1 pretreatment. Cotreatment with IGF-1R antagonist JB-1 or GPER antagonist G15 could block the neuroprotective effects of IGF-1. 1-Methy-4-phenylpyridinium (MPP+) treatment could also excessively activate autophagy along with the reduction of cell viability in SH-SY5Y cells. IGF-1 could inhibit the neurotoxicity through promoting the phosphorylation of Akt and mammalian target of rapamycin (mTOR), which could also be antagonized by JB-1 or G15. These data suggest that IGF-1 inhibits MPTP/MPP+-induced autophagy on dopaminergic neurons through the IGF-1R/PI3K-Akt-mTOR pathway and GPER.

Autophagy dysfunctions are involved in the pathogenesis of Parkinson's disease (PD). In the present study, we aimed to evaluate the involvement of G protein-coupled estrogen receptor (GPER) in the inhibitory effect of insulin-like growth factor-1 (IGF-1) against excessive autophagy in PD animal and cellular models. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment significantly induced mouse movement disorder and decreased the protein level of tyrosine hydroxylase (TH) in the substantia nigra (SN) and dopamine (DA) content in striatum. Along with the dopamine neuron injury, we observed significant upregulations of microtubule-associated light chain-3 II (LC3-II) and α-synuclein as well as a downregulation of P62 in MPTP-treated mice. These changes could be restored by IGF-1 pretreatment. Cotreatment with IGF-1R antagonist JB-1 or GPER antagonist G15 could block the neuroprotective effects of IGF-1. 1-Methy-4-phenylpyridinium (MPP

Insulin-like growth factor-1 (IGF-1) is a potent neuroprotective polypeptide that exerts neuroprotective effects via the IGF-1 receptor (IGF-1R). Our previous study reported that G protein-coupled estrogen receptor (GPER) was involved in the anti-apoptotic effect of IGF-1. The present study was designed to investigate the anti-inflammatory effect of IGF-1 in association with astrocyte activation and the molecular details of the interaction between IGF-1R and GPER. We showed that IGF-1 could improve 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor deficits and attenuate the upregulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) both in vivo and in vitro. The IGF-1R antagonist JB-1 and the GPER antagonist G15 could antagonize the anti-inflammatory effect of IGF-1. Silencing GPER abrogated the inhibitory effect of IGF-1 on 1-methyl-4-phenylpyridinium (MPP

Insulin-like growth factor-1 (IGF-1) is a potent neuroprotective polypeptide that exerts neuroprotective effects via the IGF-1 receptor (IGF-1R). Our previous study reported that G protein-coupled estrogen receptor (GPER) was involved in the anti-apoptotic effect of IGF-1. The present study was designed to investigate the anti-inflammatory effect of IGF-1 in association with astrocyte activation and the molecular details of the interaction between IGF-1R and GPER. We showed that IGF-1 could improve 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor deficits and attenuate the upregulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) both in vivo and in vitro. The IGF-1R antagonist JB-1 and the GPER antagonist G15 could antagonize the anti-inflammatory effect of IGF-1. Silencing GPER abrogated the inhibitory effect of IGF-1 on 1-methyl-4-phenylpyridinium (MPP+)-induced upregulation of COX-2 and iNOS in primary astrocytes. Moreover, the MPP + -induced inflammatory response was related to the activation of mitogen-activated protein kinases (MAPKs) and NF-κB signaling pathways. The inhibitory effects of IGF-1 on the phosphorylation of p38, JNK and IκB could be blocked by JB-1. G15 antagonized the inhibitory effects of IGF-1 on p-JNK and p-IκB, but not p-p38. Furthermore, IGF-1 treatment alone increased the expression of GPER, which was blocked by JB-1, the phosphatidylinositol 3-kinase (PI3–K) antagonist LY294002 and the MEK antagonist PD98059 in primary astrocytes. Overall, we show for the first time that GPER may contribute to the anti-inflammatory effect of IGF-1 against MPTP/MPP + -induced astrocyte activation. IGF-1 could regulate the expression of GPER via the IGF-1R/PI3-K/MAPK signaling pathway in primary astrocytes.

Insulin-like growth factor-1 (IGF-1), an endogenous peptide, exerts important role in brain development, neurogenesis and neuroprotection. There are accumulating evidence for the interaction of IGF-1 and 17β-estradiol systems. IGF-1/IGF-1 receptor (IGF-1R) signaling has been reported to regulate G-protein estrogen receptor (GPER) expression in cancer cells. Whether GPER is involved in the neuroprotective effect of IGF-1 against MPTP/MPP

Insulin-like growth factor-1 (IGF-1), an endogenous peptide, exerts important role in brain development, neurogenesis and neuroprotection. There are accumulating evidence for the interaction of IGF-1 and 17β-estradiol systems. IGF-1/IGF-1 receptor (IGF-1R) signaling has been reported to regulate G-protein estrogen receptor (GPER) expression in cancer cells. Whether GPER is involved in the neuroprotective effect of IGF-1 against MPTP/MPP+-induced dopaminergic neuronal injury remains unclear. We showed that IGF-1 could improve MPTP-induced motor deficits and ameliorate the decreased contents of DA and its metabolites in striatum as well as the loss of TH-IR neurons in the substantia nigra (SN). IGF-1 pretreatment also reversed the changes of Bcl-2 and Bax protein expressions in SN in MPTP mice. These effects were abolished by IGF-1 receptor (IGF-1R) antagonist JB-1 or GPER antagonist G15 except the inhibitory effect of G15 on Bax protein expression. Moreover, IGF-1 pretreatment enhanced cell survival against MPP+-induced neurotoxicity in SH-SY5Y cells. IGF-1 exerted anti-apoptotic effects by restoring MPP+-induced changes of Bcl-2 and Bax protein expressions as well as mitochondria membrane potential. Co-treatment with JB-1 or G15 could block these effects. Furthermore, IGF-1 regulated the protein expression of GPER through activation of phosphatidylinositol 3-kinase (PI3-K) and mitogen-activated protein kinase (MAPK) signaling pathways. Overall, we show for the first time that GPER may contribute to the neuroprotective effects of IGF-1 against MPTP/MPP+-induced dopaminergic neuronal injury.

Co2B2O5 was synthesized by the rheological phase treatment, followed by ball-milling and subsequent calcination in oxygen atmosphere. The electrochemical properties of this material as a negative electrode for lithium-ion battery were investigated. There are two plateaus with potentials at 0.83 and 0.75 V, respectively, on the first discharge curve. The initial discharge and charge capacities of Co2B2O5 are 1048 and 587 mAh g−1, respectively. The capacity retains 355 mAh g−1 after 10 cycles. The results indicate that Co2B2O5 has potential use in lithium-ion battery as a novel anode material.

A novel supramolecular resin, namely, α-(AEDPH2)·(enH2)·3H2O (1) (AEDPH2 = 1-aminoethylidenediphosphonic acid and en = ethylenediamine), is synthesized and characterized by infrared (IR) spectrosco...

A chain-shaped (H2O)4 cluster A is self-assembled in a metal phosphonate compound, [Al(phen)(AEDPH2)(AEDPH3)] · 4H2O (1) (AEDPH4 = 1-aminoethylidenediphosphonic acid, phen = 1,10-phenanthroline). This water cluster, and another chain-shaped (H2O)4 cluster B which exists in the previously reported compound [Zn(phen)(AEDPH2)2] · 4H2O (2), are investigated by X-ray crystallographic, thermal gravimetric analysis (TGA) and theoretical calculations. Both A and B collapse to ring-shaped (H2O)4 cluster C after geometry optimizations with 6-311+G(d, p) basis set at Hartree-Fock theory as well as density functional theory. Energy calculations reveal the stability is C > B > A, which is consistent with experiment results.

Lanthanum salicylate and Tb3+ -doped lanthanum salicylate were synthesized with the rheological phase reaction method. Elemental analysis, IR, TG, DTA and powder X-ray diffraction were investigated to determine the composition, crystal structure and coordination manner between the COO- and ion La3+ of lanthanum salicylate. The emission and excitation spectra of Tb3+ -doped lanthanum salicylate were also discussed. Powder X-ray diffraction suggests that the compound has a layered monoclinic structure, and the lattice parameters are a = 21.6010 A, b = 13.8015 A , c = 3.8103 A, beta = 97.11 degrees, V = 1127.2 A3, Z = 2, rhocal = 1.621 g x cm(-3) and rhoexp = 1.653 g x cm(-3). The Tb3+ -doped lanthanum salicylate exhibits very strong green luminescence of Tb3+ under the excitation of UV light. And the transition from 5D4 to 7F5 is the strongest one.

A new tailed sercine tetraphenylporphinatozinc, 5-(p-butoxyphenyl-10,15,20-trichlorophenyl)porphine and cobalt complex (Co[Ser-TPP]) was synthesized and characterized by elementary analysis, UV, IR, 1HNMR and Raman spectra. The electronic absorption spectra of axial coordination reactions of Co[Ser-TPP] with pyridine, 4-methylpyridine, 4-aminopyridine, 4,4-bipyridine, imidazole, 1-methylimidazole and 2-methylimidazole were inverstigated. The results showed that the changes of electronic absorption spectra of Co[Ser-TPP] could be attributed to the axial coordination reactions of Co[Ser-TPP] with pyridine and imidazole series.

Yttrium doped spinel LiMn2−yYyO4 with single phase was synthesized and characterized. The data of the XRD show that the limit for Y solubility is y≤0.02. The beneficial effect of Y is evident by way of improved cyclability. The electrode of LiMn1.98Y0.02O4 shows excellent electrochemical properties with a first discharge capacity of 118 mA·h·g−1 and retaining 98% of the initial capacity after 100 cycles at the current rate 0.2 C.

A novel compound, a rare earth complex oxide SnEr2O4 was synthesized by the thermal decomposition of its oxalate precursor prepared by Rheological Phase Reaction Method. TG, IR, XRD and XPS were used to prove the formation of the compound SnEr2O4. The structure of SnEr2O4 was defined by Rietveld analysis. SnEr2O4 is cubic, Pm3m, a=7.3735 A, V=400.88 A3, Z=4, Dx=8.573 g/cm3, Dm=8.2 g/cm3.