Grape Seed Procyanidin Extract Reduces Arsenic-Induced Renal Inflammatory Injury in Male Mice.

The aim of the present study is to evaluate the ability and mechanism by which grape seed procyanidin extract (GSPE) relieves arsenic trioxide (As2O3)-induced renal inflammatory injury. Therefore, male Kunming mice were treated with As2O3 and/or GSPE by gavage for 5 weeks. Mice were then sacrificed and inflammatory cytokines of kidneys were examined by ELISA, whereas the expression levels of molecules involved in the nuclear factor (NF)-κB signaling pathway were evaluated by both qRT-PCR and Western blot. Our results indicate that GSPE prevents As2O3-mediated renal inflammatory injury by inhibiting activation of the NF-κB signaling pathway and inflammatory cytokine production, while promoting expression of anti-inflammatory cytokines.

Grape Seed Proanthocyanidin Extract Alleviates Arsenic-induced Oxidative Reproductive Toxicity in Male Mice.

OBJECTIVE: To determine the ability of grape seed proanthocyanidin extract (GSPE) in alleviating arsenic-induced reproductive toxicity. METHODS: Sixty male Kunming mice received the following treatments by gavage: normal saline solution (control); arsenic trioxide (ATO; 4 mg/kg); GSPE (400 mg/kg); ATO+GSPE (100 mg/kg); ATO+GSPE (200 mg/kg) and ATO+GSPE (400 mg/kg). Thereafter, the mice were sacrificed and weighed, and the testis was examined for pathological changes. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), heme oxygenase 1 (HO1), glutathione S-transferase (GST), NAD(P)H dehydrogenase, and quinone 1 (NQO1) expression in the testis was detected by real-time PCR. Superoxide dismutase (SOD), glutathione (GSH), total antioxidative capability (T-AOC), malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), and reproductive indexes were analyzed. RESULTS: ATO-treated mice showed a significantly decreased sperm count and testis somatic index and activity levels of SOD, GSH, and T-AOC than control group. Compared to the ATO-treated group, ATO +GSPE group showed recovery of the measured parameters. Mice treated with ATO+high-dose GSPE showed the highest level of mRNA expression of Nrf2, HO, NQO1, and GST. CONCLUSION: GSPE alleviates oxidative stress damage in mouse testis by activating Nrf2 signaling, thus counteracting arsenic-induced reproductive toxicity.

[Effects of Tongbi Mixture 2 on expressions of CD28 and CD152 and content of tumor necrosis factor-alpha in peripheral blood in rats with collagen-induced arthritis].

OBJECTIVE: To study the effects of Tongbi Mixture 2, a compound traditional Chinese herbal medicine for treating rheumatoid arthritis (RA), on immunoregulation of T lymphocytes in rats with collagen-induced arthritis (CIA). METHODS: Forty Wistar rats were randomly divided into normal control group, untreated group, Tongbi Mixture 2-treated group, methotrexate (MTX)-treated group and Tripterygium wilfordii polyglycoside (TWP)-treated group. Except for the rats of the normal control group (injection with normal saline), rats of the other four groups were subcutaneouly multipoint-injected with collagen protein II to induce CIA. The rats were treated with normal saline, Tongbi Mixture 2, MTX tablets and TWP tablets respectively for 36 days. The expressions of CD28 and CD152 were detected by flow cytometry, while the content of tumor necrosis factor-alpha (TNF-alpha) was analyzed by enzyme-linked immunosorbent assay. RESULTS: The expression of CD28 among the three drug treated groups had no statistical difference (P>0.05), while significantly higher than that of the normal control group (P<0.01) and lower than that of the untreated group (P<0.01). The expression of CD152 in the Tongbi Mixture 2 treated-group was lower than those of the MTX- and TWP-treated groups (P<0.05, P<0.01), but had no statistical difference as compared with the normal control group (P>0.05). There were no statistical differences in content of TNF-alpha between the drug treated groups and the normal control group (P>0.05), but the content of TNF-alpha of the drug treated groups was lower than that of the untreated group (P<0.05 or P<0.01). CONCLUSION: Tongbi Mixture 2 can inhibit T lymphocytes through down-regulating the expressions of CD28 and CD152 and the content of TNF-alpha, which may be the major mechanisms in treating RA.