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The appearance of Solanum nigrum L. nigrum.

The appearance of Solanum nigrum L. nigrum.

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Previously, the Solanum nigrum polysaccharide fraction, SN-ppF3 was proven to have an immunomodulatory activity by classically activating RAW 264.7 murine macrophage cell line. However, the cellular pathway induced by SN-ppF3 has not to be outlined. In the present study, we predicted the possible cellular pathways induced when macrophage cells were...

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... plants of Solanum nigrum L. nigrum (Figure 1) were purchased from the local market in Lembah Pantai, Kuala Lumpur, Malaysia. The plants were identified and authenticated by Dr. Sugumaran Manickam from Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia, and a voucher specimen was deposited at the Rimba Ilmu Herbarium (Herbarium number: KLU 47872). ...

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... S. nigrum is commonly used as traditional folk medicine and is believed to have various biological activities such as anti-cancer, anti-septic, anti-dysenteric and wound healing properties 5 . In the previous studies, the S. nigrum polysaccharide fraction, SN-ppF3 was proven to have immunomodulatory activities where it could classically activate macrophage cells through the NF-êB transduction signaling pathway and indirectly suppressed the proliferation of breast cancer cells in tumor-induced BALB/c mice 6,7,8 . These documented health benefits of the S. nigrum plant products can be utilized in various pharmaceutical applications. ...
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The polysaccharide isolated from Solanum nigrum was proven to possess an immunomodulatory effect and able to suppress the progression of tumor cells by proxy. However, data on the toxicity profile is still limited. The present preclinical study was conducted to investigate the toxicity potential of the crude polysaccharide sample. The acute toxicity experimental design was adapted from OECD 423 guideline. Nine female BALB/c mice were randomly divided into 3 groups, 3 mice per group (n=3). Mice in group A (first-step treatment) were orally administered with a single treatment of crude polysaccharide sample at concentration 2,000 mg/kg/bw (300 µL). Mice in group B (second-step treatment) were received the single treatment after 24 hours, depending on the observation of mice in group A. Mice in group C served as control. Mortality and clinical signs associated with toxicity were observed within 24 hours of treatment session and for the subsequence 14 days for delay-death detection. Mice body weight was recorded starting at day-0 until day-14 prior to sacrificing at day-15. Blood, liver, and kidney were harvested for toxicology assessment. Within 24 hours of treatment, 1 mouse in group A was found to died, while no mortality and delay-death were observed in groups B and C. Referring to OECD 423, it was estimated that the LD50 of the treated sample was 2,500–5,000 mg/kg/bw. No significant changes (p<0.05) were detected in terms of body weight and organ weight indexes of the treated mice as compared to control. The polysaccharide treatment also revealed no significant elevation in mice serum glucose levels. The present findings indicated that the treatment of crude polysaccharide sample exerted a very mild acute toxicity effect when orally administered at 2,000 mg/kg/bw, with no delay-death.