A new benzamide derivative from rice fermentation of Streptomyces sp. CPCC 202950 / 中国中药杂志

Eight compounds were isolated from the rice fermentation of Streptomyces sp. CPCC 202950 by a combination of various chromatographic techniques including column chromatography over silica, Sephadex LH-20, flash C₁₈, and reversed-phase HPLC. Their structures were identified as 3-[(3'-amino-3'-oxoprop-1'-en-2'-yl)oxy]benzamide (1), m-hydroxybenzamide (2), leptosphaepin (3), 5-methyluracil (4), feruloylamide (5), p-hydroxyphenylacetoamide (6), vanillamide (7), cyclo (L-val-L-ala) (8). Among them, 1 was a new benzamide analogue, and 2 was a new natural product. In the preliminary assays, none of the compounds 1-8 exhibited obvious inhibition of HIV-1 protease activity, and toxic with the Hela, HepG2, and U2OS cells. (IC₅₀ > 10 μmol•L⁻¹).

Effects of subchronic benzoapyrene exposure on hippocampal cholinergic system in rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the effects of subchronic benzo[a]pyrene (B[a]P) exposure on the neurobehavior and hippocampal acetylcholine (Ach) level, acetylcholinesterase (AChE) activity, and mRNA and protein expression of nicotinic acetylcholine receptor α7 subtype (nAChR α7) in rats, and to investigate the neurotoxic mechanism of B[a]P.</p><p><b>METHODS</b>Sixty healthy male SD rats were randomly divided into blank control group, solvent control group, and B [a]P exposure groups. Each rat in the exposure groups was intraperitoneally injected with B[a]P at 1.0, 2.5, or 6.25 mg/kg once every other day for 90 days. The learning and memory ability of the rats was examined by Morris water maze test and step-down test; the hippocampal Ach level was measured by alkaline hydroxylamine method; the AChE activity was measured by DNTB method; the mRNA and protein expression levels of hippocampal nAChR α7 were measured by quantitative PCR and Western blot.</p><p><b>RESULTS</b>The 2.5 and 6.25 mg/kg B[a]P exposure groups showed significantly lower learning and memory abilities than the blank control group and solvent control group (P < 0.05); also, the two groups had significantly lower hippocampal Ach levels than the blank control group, solvent control group, and 1.0 mg/kg B[a]P exposure group (P < 0.05). The 6.25 mg/kg B[a]P exposure group showed significantly lower hippocampal AChE activity than the blank control group, solvent control group, and 1.0 mg/kg B[a]P exposure group (P < 0.05). There were no significant differences in the mRNA and protein expression levels of nAChR α7 among all groups (P > 0.05). The hippocampal Ach level was negatively correlated with the mean escape latency period and total distance travelled (r = -0.567, P < 0.01; r = -0.503, P < 0.01) but positively correlated with the time in platform quadrant (r = 0.800, P < 0.01).</p><p><b>CONCLUSION</b>Subchronic B[a]P exposure may impair the learning and memory ability in rats, which is related to the downregulation of hippocampal Ach level.</p>

The modification of apoptosis correlated gene, protein and protein activity in rat hippocampus induced by benzoa pyrene sub-chronic exposure / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the effects of subchronic exposure to benzo[a]pyrene (B[a]P) on the mRNA and protein expression levels of apoptosis-related genes (bax, bcl-2, caspase-3, caspase-6, and caspase-9) and the activities of Caspase-3, Caspase-6, and Caspase-9 in the hippocampal neurons of rats and to investigate the neurotoxic mechanism by which B[a]P induces the apoptosis of neurons.</p><p><b>METHODS</b>Fifty-two healthy SD rat were randomly divided into five groups according to preliminary neurobehavioral test results: blank control group, solvent control group, and 1.0, 2.5, and 6.25 mg/kg B[a]P exposure groups; the rats in exposure groups were intraperitoneally injected with B[a]P every other day for 90 days. The Morris water maze was used to test the learning and memory ability of rats; flow cytometry was used to measure the apoptosis ratio of hippocampal neurons; real-time quantitative PCR and Western blot were used to measure the mRNA and protein expression levels of apoptosis-related genes; spectrophotometry was used to measure the activities of their en-coded proteins.</p><p><b>RESULTS</b>Compared with the blank control group, solvent control group, and 1.0 mg/kg B[a]P exposure group, the 2.5 and 6.25 mg/kg B[a]P exposure groups hada significantly longer mean escape latency period (P < 0.05) and a significantly increased number of times of platform crossing (P < 0.05), and the 6.25 mg/kg B[a]P exposure group had significantly lower length and percentage of time spent in the platform quadrant (P < 0.05). The early apoptosis ratio rose as the dose of B[a]P increased (P trend < 0.05); the early apoptosis ratios of 1.0, 2.5, and 6.25 mg/kg B[a]P exposure groups were significantly higher than those of blank control group and solvent control group (P < 0.05). Compared with the blank control group, solvent control group, and 1.0 and 2.5 mg/kg B[a]P exposure groups, the 6.25 mg/kg B[a]P exposure group had significantly increased Bax expression (P < 0.05) and significantly decreased Bcl-2 expression and Bcl-2/Bax ratio (P < 0.05). The 2.5 and 6.25 mg/kg B[a]P exposure groups had significantly higher expression levels of Caspase-3 and Caspase-6 than the blank control group, solvent control group, and 1.0 mg/kg B[a]P exposure group (P < 0.05). The activities of Caspase-3, Caspase-6, and Caspase-9 were significantly higher in the 2.5 and 6.25 mg/kg B[a]P exposure groups than in the blank control group and solvent control group (P < 0.05). There was a positive correlation between the activities of Caspase-3, Caspase-6, and Caspase-9 and early apoptosis ratio of hippocampal neurons in rats (r = 0.793, P = 0.019; r = 0.886, P = 0.006; r = 0.773, P = 0.025). There were no significant differences in the mRNA expression of Bax, Bcl-2, Caspase-3, Caspase-6, and Caspase-9 among these groups (P > 0.05).</p><p><b>CONCLUSION</b>Subchronic exposure to B[a]P can induce apoptosis of hippocampal neurons; its mechanism may be related to the fact that B[a]P can induce upregulated expression of Bax, inhibit expression of Bcl-2, lead to decrease in Bcl-2/Bax ratio, induce upregulated expression of Caspase-3 and Caspase-6, and cause increase in the activities of Caspase-3, Caspase-6, and Caspase-9.</p>

Effect of Ganoderma lucidum polysaccharides on oxidative stress of hyperlipidemic fatty liver in rats / 中国中药杂志

<p><b>OBJECTIVE</b>To study the effect of Ganoderma lucidum polysaccharides on oxidative stress of hyperlipidemic fatty liver in rats.</p><p><b>METHOD</b>Seventy-two SD rats were randomly divided into six groups, namely the normal control group (NG), the model group (MG), the G. lucidum polysaccharides groups of low, middle and high dose (GLPs-LG, GLPs-MG, GLPs-HG) and the Simvastatin group (SV). The rats were fed with high fat diet to establish the model of hyperlipidemic fatty liver in rats. After administration for 12 weeks, rats in each group were tested with the following indexes: total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) in serum as well as the contents of SOD, MDA, GSH-Px and T-AOC in hepatic tissues. Histopathological changes of hepatic tissues were observed under light glass.</p><p><b>RESULTS</b>The contents of TC, TG and LDL-C were significantly increased in the model group (P < 0.01). Compared with the model group, both the GLPs-M group and the GLPs-H group showed significant decreases in TC, TG and LDL-C (P < 0.05 or P < 0.01), while the GLPs-H group showed a notable increase in HDL-C (P < 0.05). Compared with the model group, both the GLPs-M group and the GLPs-H group showed significant decreases in MDA (P < 0.05 or P < 0.01) and notable increases in SOD, GSH-Px, T-AOC (P < 0.05 or P < 0.01). The GLPs-M group and the GLPs-H group proved a remarkable alleviation in fatty degeneration of hepatic cells.</p><p><b>CONCLUSION</b>G. lucidum polysaccharides can significantly reduce the blood fat level of hyperlipidemic fatty liver in rats and effectively inhibit oxidant stress, showing the effect on preventing and treating hyperlipidemic fatty liver in rats to some extent.</p>