PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27989594-4 2017 Moreover, SalB treatment ameliorated ethanol-induced hepatic inflammation by decreasing the levels of hepatotoxic cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). salvianolic acid B 10-14 tumor necrosis factor Rattus norvegicus 132-159 31790900-7 2020 RESULTS: Salvianolic acid B significantly decreased the expressions of TXB2 and ET-1 and increased the expression of 6-keto-PGF1alpha in plasma, and significantly inhibited the overexpression of TNF-alpha and iNOS in the femoral artery walls of TAO rats at medium and high doses. salvianolic acid B 9-27 tumor necrosis factor Rattus norvegicus 195-204 27989594-4 2017 Moreover, SalB treatment ameliorated ethanol-induced hepatic inflammation by decreasing the levels of hepatotoxic cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). salvianolic acid B 10-14 tumor necrosis factor Rattus norvegicus 161-170 18215345-6 2008 Sal B was used to protect MSC from being damaged by TNF-alpha in vitro. salvianolic acid B 0-5 tumor necrosis factor Rattus norvegicus 52-61 25981395-11 2015 SalB also exerted anti-inflammatory effects as indicated by the decreased TNF-alpha and IL-1beta levels in the brain tissue. salvianolic acid B 0-4 tumor necrosis factor Rattus norvegicus 74-83 23943397-11 2013 The expression of pro-inflammatory factors TNF-alpha and NF-kappaB was found to be greatly increased 24 h post-SCI, and this upregulation was significantly attenuated by Sal B treatment. salvianolic acid B 170-175 tumor necrosis factor Rattus norvegicus 43-52 22101700-18 2011 The protective effects of Sal B may be through inhibiting the TLR4-NFkappaB-TNFalpha pathway and are dose-dependent. salvianolic acid B 26-31 tumor necrosis factor Rattus norvegicus 76-84 20238162-2 2010 Our results showed that Sal B significantly reduced the production of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and reactive oxygen species (ROS) induced by lipopolysaccharide (LPS) treatment in rat primary microglia in a dose-dependent manner. salvianolic acid B 24-29 tumor necrosis factor Rattus norvegicus 89-116 20238162-2 2010 Our results showed that Sal B significantly reduced the production of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and reactive oxygen species (ROS) induced by lipopolysaccharide (LPS) treatment in rat primary microglia in a dose-dependent manner. salvianolic acid B 24-29 tumor necrosis factor Rattus norvegicus 118-127 20238162-4 2010 Sal B also suppressed LPS-induced inducible nitric oxide synthase (iNOS), TNF-alpha, and IL-1beta mRNA expression, which was accompanied by inhibiting transcription factor NF-kappaB activation. salvianolic acid B 0-5 tumor necrosis factor Rattus norvegicus 74-83 28852731-7 2016 RESULTS: Sal B significantly improved heart function and decreased infarct size; remarkably decreased levels of serum TNF-alpha and IL-Iotabeta levels, increased contents of myocardium antioxidant enzymes activities; western blot results showed that Sal B ameliorate the increased Bax and caspase-3 protins expressions and decreased Bcl-2 proteins expression and ratios of Bcl-2 to Bax. salvianolic acid B 9-14 tumor necrosis factor Rattus norvegicus 118-127 22101700-0 2011 Salvianolic acid B inhibits the TLR4-NFkappaB-TNFalpha pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide. salvianolic acid B 0-18 tumor necrosis factor Rattus norvegicus 46-54 22101700-10 2011 Compared with the LPS control group, the concentrations of LDH and TNFalpha were significantly decreased in the Sal B 10(-5)mol/L pre-treated group (451.76+-83.96 U/L and 34.00+-10.38 pg/mL, respectively, P<0.05). salvianolic acid B 112-117 tumor necrosis factor Rattus norvegicus 67-75 18215345-10 2008 MSC were protected from the damage of TNF-alpha by Sal B. salvianolic acid B 51-56 tumor necrosis factor Rattus norvegicus 38-47