rhein/atrophy

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In vitro deterioration of rhein anthraquinone in cecal content of rats.

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The influence of the intestinal microbial reduction of rhein anthraquinone on the formation of deterioration products was studied. Therefore [14C]rhein and [14C]rhein anthrone were mixed with sterilized or non-sterilized cecal mass of rats and incubated for 20 hours at 37 degrees C. Extractions with

Rhein: a potential biological therapeutic drug for intervertebral disc degeneration.

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Intervertebral disc degeneration (IDD) is regarded as an important cause of low back pain, which continues to be a common disability. IDD is thought to involve sequential changes of intervertebral disc that lead to the reduction of disc cells and the extracellular matrix. In addition, inflammation

Dynamic influence of Rhein lysinate on HeLa cells.

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In a previous study, it was demonstrated that Rhein lysinate (RHL) inhibited HeLa cell proliferation via a specific mechanism. The aim of the present study was to clarify the mechanism of RHL by investigating its effect on mitochondrial damage and cell apoptosis. The results indicated that RHL

Rhein laden pH-responsive polymeric nanoparticles for treatment of osteoarthritis

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Osteoarthritis (OA) is a condition associated with severe inflammation, cartilage destruction and degeneration of joints. Rhein (Rh) is an effective anti-inflammatory drug with proven efficacy in in-vitro and in-vivo models. pH sensitive Rh and NH₄HCO₃ laden poly

Rhein alleviates renal interstitial fibrosis by inhibiting tubular cell apoptosis in rats.

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Ureteral obstruction causes injury of the renal tissues and can irreversibly progress to renal fibrosis, with atrophy and apoptosis of tubular cells. The goal of the current study was to examine the effects of rhein on the apoptosis o renal tubular cells as well as renal fibrosis using

Rhein lysinate induced S-phase arrest and increased the anti-tumor activity of 5-FU in HeLa cells.

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Rhein lysinate (RHL), easily dissolved in water, is one of the anthraquinones, and has been shown to have anti-tumor activity in different human cancer cell lines. In the present study, we observed that RHL could cause vacuolar degeneration in HeLa cells, which was not observed in human umbilical

Rhein protects against acetaminophen-induced hepatic and renal toxicity.

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This study investigated the possible protective effects and mechanism of rhein on Acetaminophen (APAP)-induced hepatotoxicity and nephrotoxicity in rats. Treatment of rats with APAP resulted in severe liver and kidney injuries, as demonstrated by drastic elevation of serum glutamate-pyruvate

Rhein Elicits In Vitro Cytotoxicity in Primary Human Liver HL-7702 Cells by Inducing Apoptosis through Mitochondria-Mediated Pathway.

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Objective. To study rhein-induced apoptosis signaling pathway and to investigate its molecular mechanisms in primary human hepatic cells. Results. Cell viability of HL-7702 cells treated with rhein showed significant decrease in dose-dependent manner. Following rhein treatment (25 μM, 50 μM, and 100

Self-nanoemulsifying drug-delivery systems for potentiated anti-inflammatory activity of diacerein.

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UNASSIGNED Effective treatment of osteoarthritis necessitates both symptomatic relief and hindrance of joint degeneration progression. Non-steroidal anti-inflammatory drugs permit symptomatic relief only and can cause mucosal injury in the gut. Before absorption, diacerein (Dcn) is converted into

Anthraquinone-2,6-disulfonic acid as a disease-modifying osteoarthritis drug: an in vitro and in vivo study.

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Pharmacologic treatment of osteoarthritis has been confined mostly to analgesic or nonsteroidal antiinflammatory drugs that only modify the symptoms. We asked whether anthraquinone-2,6-disulfonic acid might act as a disease-modifying osteoarthritis drug. We evaluated the in vitro inhibitory effect

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