Gelatin microspheres encapsulated with a nonpeptide angiogenic agent, ginsenoside Rg1, for intramyocardial injection in a rat model with infarcted myocardium

Wei, Hao-Ji; Yang, Hang-Hsing; Chen, Chun‐Hung; Lin, Wei-Wen; Chen, Sung-Ching; Lai, Po-Hong; Chang, Yen; Sung, Hsing‐Wen

doi:10.1016/j.jconrel.2007.04.005

Cited by 54 publications

(41 citation statements)

References 47 publications

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“…11,12 In addition, Xie et al elaborated that G-Rg1 ameliorated renal interstitial fibrosis by inhibiting the tubular epithelial-myofibroblast transition 27 and decreasing the expression of thrombospondin-1.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 Ginsenoside-Rg1 (G-Rg1) is believed to be the main active component of Panax ginseng, a traditional Chinese herb, which poses antioxidant, anti-proliferative and anti-apoptotic activities and is used extensively to treat neurological, cardiovascular, hepatic and inflammation or immune related diseases. 9,10 Related studies demonstrate that G-Rg1 can markedly inhibit organ fibrosis, including myocardial fibrosis 11 and liver fibrosis. 12 The anti-fibrotic activity of G-Rg1 on renal fibrosis has been studied as well.…”

Section: Introductionmentioning

confidence: 99%

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Ginsenoside-Rg1 inhibits endoplasmic reticulum stress-induced apoptosis after unilateral ureteral obstruction in rats

Deng

et al. 2015

Renal Failure

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(2015) Ginsenoside-Rg1 inhibits endoplasmic reticulum stress-induced apoptosis after unilateral ureteral obstruction in rats, Renal Failure, 37:5,[890][891][892][893][894][895] DOI: 10.3109 Aim: Endoplasmic reticulum (ER) stress and unfolded protein response (UPR) are implicated in many fibrotic diseases, including renal fibrosis. Whether Ginsenoside-Rg1 (G-Rg1) could attenuate renal fibrosis via suppression of ER stress and UPR has not been reported. The aim of this study was to explore the effect of G-Rg1 on ER stress and UPR-induced apoptosis in kidneys with unilateral ureteral obstruction (UUO) rat model. Methods: Twenty-four male SpragueDawley rats were randomly divided into control group, model group and G-Rg1 treatment group. G-Rg1 was administered to rats by intraperitoneal injection. Renal interstitial fibrosis in the model group was developed by UUO in rats. Renal function was estimated by the levels of serum creatinine (Scr) and blood urea nitrogen (BUN). Renal pathological damage was evaluated by hematoxylin and eosin (HE) and Masson's trichrome staining. The ER stress was assessed with glucose-regulated protein (GRP) 78 expression, and the proapoptotic response was detected with CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase-12 expressions by Western Blot. The number of apoptotic cells was determined by Terminaldeoxynucleotidyl Transferase Mediated Nick End Labeling (TUNEL) analysis. Results: UUO for 14 days aggravated renal function, renal damage and renal interstitial fibrosis, activated ER stress response (induction of GRP78 protein), enhanced the proapoptotic response (increase in CHOP and caspase-12 proteins) and increased the number of apoptotic cells (shown by the TUNEL assay). Treatment with G-Rg1 significantly ameliorates the renal pathological lesions and decreases expressions of ER stress-associated proteins and the level of apoptotic cells in kidneys. Conclusion: G-Rg1 suppresses renal cell apoptotic and fibrotic process partly through inhibition of ERS-and UPR-related apoptotic pathway in the kidneys after UUO.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ginsenoside-Rg1 inhibits endoplasmic reticulum stress-induced apoptosis after unilateral ureteral obstruction in rats

Deng

et al. 2015

Renal Failure

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“…A reticulação das esferas com GP foi realizada segundo metodologia proposta por Magalhães Jr e colaboradores [30] , Barck e Butler [31] e Wei e colaboradores [32] . Para esta modificação química, as esferas ainda úmidas foram imersas em solução de GP 100 mmol/L em etanol 90%, sob agitação lenta por 24 h. Ao final deste período, as esferas foram lavadas exaustivamente com água deionizada e secas ao ar a 25 °C.…”

Section: Efeito Da Modificação Química Na Solubilidade E Intumescimenunclassified

Efeito da modificação química na solubilidade e intumescimento de microesferas à base de goma do cajueiro carboximetilada e quitosana

et al. 2015

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ResumoEsferas de goma do cajueiro carboximetilada e quitosana foram produzidas via complexação polieletrolítica. As esferas foram modificadas quimicamente de modo a obter-se sistemas estáveis em meio ácido e que apresentassem uma resposta de intumescimento diferenciado frente à variação de pH. As esferas foram modificadas por reacetilação da quitosana e por reticulação com epicloridrina, glutaraldeído e genipina. As esferas reticuladas foram caracterizadas por meio de técnicas como: espectroscopia de absorção no infravermelho, análise termogravimétrica, microscopia eletrônica de varredura e quanto à solubilidade em pH 1,2 e ao intumescimento. As esferas de goma do cajueiro carboximetilada e quitosana reacetilada, e as esferas reticuladas com epicloridrina apresentaram baixa resistência à dissolução em pH 1,2. Entretanto, as esferas reticuladas com glutaraldeído e genipina apresentaram resistência à dissolução e baixo coeficiente de difusão. As esferas reticuladas com genipina apresentaram um grau de intumescimento maior do que as esferas reticuladas com glutaraldeído nas concentrações de 3% e 5% (massa/volume). As esferas reticuladas com genipina apresentaram intumescimento responsivo à variação de pH e estabilidade em pH 1,2, indicando que esses sistemas possuem potencial para uso em sistemas de liberação controlada de fármacos por via oral. PalavrasTchave: goma do cajueiro, carboximetilação, quitosana, reticulação. AbstractChitosan/carboxymethylated cashew gum beads were produced via polyelectrolytic complexation. The beads were chemically modified to achieve stable acidic medium and to provide a swelling response in different pH. The beads were modified by chitosan reacetylation and by crosslinking with epichlorohydrin, glutaraldehyde and genipin. The beads were characterized by techniques such as: infrared spectroscopy, thermogravimetry, scanning electron microscopy and regarding their solubility at pH 1.2 and swelling. The beads of carboxymethyl cashew gum and reacetylated chitosan and those crosslinked with epichlorohydrin had low resistances to dissolution at pH 1.2. However, the beads crosslinked with glutaraldehyde and genipin showed resistance to dissolution along with low diffusion coefficients. Moreover, beads crosslinked with genipin presented a higher degree of swelling than beads crosslinked with glutaraldehyde at concentrations of 3% and 5% (weight/volume). Beads crosslinked with genipin presented responsive behavior to pH variation and stability at pH 1.2, indicating that these systems have potential for use in controlled drug delivery systems for oral administration.

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“…Yu et al (32) have also demonstrated that the antioxidant defense system against exercise-induced oxidative stress is strengthened by oral supplements of Rg1 in rat skeletal muscle. However, the function of Rg1 in the resistance to muscle atrophy remains unclear (33)(34)(35)(36)(37)(38).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 prevents starvation-induced muscle protein degradation via regulation of AKT/mTOR/FoxO signaling in C2C12 myotubes

Peng

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Skeletal muscle atrophy is often caused by catabolic conditions including fasting, disuse, aging and chronic diseases, such as chronic obstructive pulmonary disease. Atrophy occurs when the protein degradation rate exceeds the rate of protein synthesis. Therefore, maintaining a balance between the synthesis and degradation of protein in muscle cells is a major way to prevent skeletal muscle atrophy. Ginsenoside Rg1 (Rg1) is a primary active ingredient in Panax ginseng, which is considered to be one of the most valuable herbs in traditional Chinese medicine. In the current study, Rg1 was observed to inhibit the expression of MuRF-1 and atrogin-1 in C2C12 muscle cells in a starvation model. Rg1 also activated the phosphorylation of mammalian target of rapamycin (mTOR), protein kinase B (AKT), and forkhead transcription factor O, subtypes 1 and 3a. This phosphorylation was inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. These data suggest that Rg1 may participate in the regulation of the balance between protein synthesis and degradation, and that the function of Rg1 is associated with the AKT/mTOR/FoxO signaling pathway. IntroductionMuscle atrophy is characterized by an increase in protein degradation and reduction in protein synthesis. It is associated with a number of human diseases and catabolic conditions, including fasting, disuse, aging, cancer, neuromuscular diseases, stroke, chronic obstructive pulmonary disease, chronic heart failure, HIV-acquired immunodeficiency syndrome and sepsis (1-5). Muscle volume shrinking and muscle weakness induced by muscular dystrophy typically disrupt and adversely affect the life of patients (3,6-8). Therefore, it is essential to understand the mechanism by which skeletal muscle atrophy is regulated.A large amount of protein hydrolysis has previously been identified to occur during muscle atrophy and the ubiquitin-proteasome system (UPS) has been demonstrated to be involved in this process (9)(10)(11)(12)(13)(14). In this system, the proteins are first conjugated into multiple molecules of ubiquitin. The 26S proteasome then recognizes and degrades the ubiquitinated proteins (15,16). Multiple enzymes regulate the protein ubiquitination; these include E1, the ubiquitin-activating enzyme, E2, the ubiquitin conjugating enzyme and E3 ubiquitin ligases (17,18). E3 ubiquitin ligases serve a major role in the specificity of protein degradation, because the specific binding between the protein substrate and E3 occurs prior to the reaction with ubiquitin (18,19).It has been demonstrated that the insulin-signaling pathway is involved in the inhibition of UPS (20). In this pathway, the phosphorylation of insulin receptor substrate is stimulated when insulin binds its receptor. Phosphatidylinositol 3-kinase (PI3K), an intracellular intermediate, is recruited to phosphorylate a serine/threonine kinase, protein kinase B (AKT) during this process. AKT then phosphorylates the forkhead box class O transcription factors, subtype 1 and 3a (FoxO1 and FoxO3a), which pre...

show abstract

Gelatin microspheres encapsulated with a nonpeptide angiogenic agent, ginsenoside Rg1, for intramyocardial injection in a rat model with infarcted myocardium

Cited by 54 publications

References 47 publications

Ginsenoside-Rg1 inhibits endoplasmic reticulum stress-induced apoptosis after unilateral ureteral obstruction in rats

Ginsenoside-Rg1 inhibits endoplasmic reticulum stress-induced apoptosis after unilateral ureteral obstruction in rats

Efeito da modificação química na solubilidade e intumescimento de microesferas à base de goma do cajueiro carboximetilada e quitosana

Ginsenoside Rg1 prevents starvation-induced muscle protein degradation via regulation of AKT/mTOR/FoxO signaling in C2C12 myotubes

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