PHYSICOCHEMICAL CHARACTERIZATION OF AN HEMAGGLUTINATING PROTEIN FROM THE FRUIT OF Cola nitida, KOLANUT

This study partially purified and characterized an hemagglutinating protein from the fruit of Cola nitida. This protein had heamagglutinating activity towards human erythrocytes (ABO system) and was non-blood group specific. The activity was stable at pH range of 5 – 12, and was inhibited at pHs 3 and 4. The lectin activity was heat stable up to 70 °C and was not inhibited by chelating with EDTA

Syringic acid demonstrates an anti-inflammatory effect via modulation of the NF-κB-iNOS-COX-2 and JAK-STAT signaling pathways in methyl cellosolve-induced hepato-testicular inflammation in rats

Syringic acid (SACI) is an emerging nutraceutical and antioxidant used in modern Chinese medicine. It has potential neuroprotective, anti-hyperglycemic, and anti-angiogenic properties. Methyl cellosolve (MCEL) has been reported to induce tissue inflammation in the testis, kidney, liver, and lung. This study aimed to investigate the effect and probable mechanism of action of SACI on MCEL-induced hepatic and testicular inflammation in male rats. Compared to the control group, administration of MCEL to rats significantly increased the levels of IL-6, TNF-α, iNOS, COX-2, and NF-κB in the liver and testis. Additionally, the total mRNA expressions of JAK1 (in the liver only), STAT1, and SOCS1 were significantly increased in both the liver and testis, while testicular JAK1 total mRNA levels were significantly decreased.The expression of PIAS1 protein was significantly higher in the liver and testis. Treatments with SACI at 25 (except liver iNOS), 50, and 75 mg/kg significantly decreased the levels of IL-6, TNF-α, iNOS, COX-2, and NF-κB compared to the control group. Furthermore, the total mRNA expressions of JAK1 and SOCS1 in the liver were significantly reduced by all doses of SACI investigated, while the total mRNA levels of liver and testis STAT1 were significantly reduced by 25 and 50 mg/kg of SACI only. In the testis, the mRNA level of SOCS1 was significantly reduced by all doses of SACI compared to MCEL only. Additionally, SACI (at 75 mg/kg) significantly reduced PIAS1 protein expression in the liver, while in the testis, SACI at all investigated doses significantly reduced the expression of PIAS1. In conclusion, SACI demonstrated a hepatic and testicular anti-inflammatory effect by inhibiting the MCEL-induced activation of the NF-κB and JAK-STAT signaling pathways in rats

Methyl cellosolve-induced hepatic oxidative stress: The modulatory effect of syringic acid on Nrf2-Keap1-Hmox1-NQO1 signaling pathway in rats

Ethnopharmacological relevance: Syringic acid (SAC) is a phenolic compound and an antioxidant that has been identified in honey, grapes, red wine, marigold and sugar apple. Due to its potent antioxidant prowess, SAC possesses hepatoprotective, nephroprotective, neuroprotective, cardioprotective and anti-inflammatory activities. Aim of the study: Judging by these credentials, this study investigated the effect of 25, 50 and 75 mg/kg body weight of SAC on hepatotoxicity induced by 100 mg/kg body weight of methyl cellosolve (MECE) in male Wistar rats. Results: Compared with control, MECE decreased the liver relative weight, nitric oxide (NO) concentration, glutathione S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD) activities, while liver malondialdehyde (MDA), nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH associated protein 1 (Keap1), heme oxygenase 1 (Hmox1) and NAD(P)H quinone oxidoreductase 1 (NQO1) levels were significantly increased. Treatments with 25, 50 and 75 mg/kg of SAC significantly decreased the concentration of MDA, Nrf2, Keap1 (by 50 and 75 mg/kg only), mRNA expressions of Hmox1, NQO1 and increased the concentration of NO, activities of GPx, GST, SOD and CAT compared with MECE only administered rats. Conclusion: In conclusion, SAC demonstrated a strong hepatoprotective role against MECE-induced hepatic depletion of endogenous antioxidant enzymes and inhibition of MECE-induced cytosolic Nrf2 activation and antioxidant response element (ARE)-dependent genes in rats