OBJECTIVE:To further exploit the active components from Loquat leaf and its gruffs.METHODS:The chief components in loquat leaf and its gruffs were extracted by ultrasound extraction and Soxhlet extraction,respectively,the sepa?ration of ursolic acid and other constituents was performed by HPLC,and the relative amounts of which were determined and compared.RESULTS:Soxhlet extraction is superior to ultrasound extraction in the extraction of loquat leaf and8components in gruffs.Under the same extraction method,the content of ursolic acid in loquat leaves is equivalent to that of gruffs.Besides,the contents of6components in gruffs were above those in loquat leaves.CONCLUSION:The essential component-triterpenic acid in loquat leaves suffered no loss after extraction with water,the active components in gruffs can be further exploited.

Objective To investigate the effect of resveratrol (Res) on paraquat (PQ)-induced acute lung injury (ALI) and mortality in mice and the mechanism of nuclear factor-κB (NF-κB) inflammatory pathway. Methods Sixty-eight healthy male ICR mice with grade SPF were enrolled, among them 20 mice were used for mortality observation (n = 10), and other 48 were used for determination of related parameters (n = 6). The mice were randomly divided into four group s: normal saline (NS) control group, Res control group, PQ group and PQ + Res group. The mice in the latter two groups were subdivided into 6, 24, 72 hours subgroups. The PQ poisoning model of mice was reproduced by one injection of 30 mg/kg PQ intraperitoneally. The mice in PQ + Res group were given 60 mg/kg Res intraperitoneally on the contralateral side after PQ injection. The mice were sacrificed at 6, 24, 72 hours after PQ poisoning, and lung tissue was harvested. The serum levels of tumor necrosis factor-α (TNF-α), interleukins (IL-6 and IL-1β) were determined by enzyme linked immunosorbent assay (ELISA). The pathological changes in lung tissue were observed with electron microscopy. Apoptosis cells in the lung were identified by terminal dexynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) for the estimation of apoptosis rate. The protein expression of NF-κB p65 was determined by Western Blot. Results Compared with PQ group, the death number of mice at 48, 72, 96 hours in PQ + Res group was slightly decreased (0 vs. 2, 2 vs. 5, 4 vs. 6) but without statistically significant difference (all P > 0.05). Under electron microscope, the lung injury in PQ group was severer than that in NS control group, and Res was found to be able to alleviate the lung injury. Compared with NS control group [(2.45±0.61)%], the apoptosis rate at 6 hours in PQ group was significantly increased [(8.42±1.48)%], and peaked at 72 hours [(21.23±3.47)%]. Res could decrease the apoptosis rate after PQ poisoning [6 hours: (5.56±1.31)% vs. (8.42±1.48)%, 24 hours: (11.14±2.07)% vs. (16.88±2.96)%, 72 hours: (13.28±2.32)% vs. (21.23±3.47)%, all P < 0.05]. The serum levels of TNF-α, IL-6, and IL-1β, and NF-κB p65 in lung tissue were all markedly increased after PQ poisoning, and they were significantly decreased after Res intervention as compared with those of PQ group [TNF-α (ng/L): 2.62±0.29 vs. 4.06±0.74 at 6 hours, 3.98±0.41 vs. 6.79±0.80 at 24 hours, 5.06±0.75 vs. 11.00±0.75 at 72 hours; IL-6 (ng/L): 14.19±1.54 vs. 16.55±1.24 at 6 hours, 13.21±1.37 vs. 19.73±0.85 at 24 hours, 13.72±0.56 vs. 22.45±0.72 at 72 hours; IL-1β (ng/L): 8.54±1.64 vs. 12.59±0.66 at 6 hours, 10.15±0.29 vs. 16.24±1.03 at 24 hours, 16.14±0.70 vs. 19.55±0.56 at 72 hours; 6-hour NF-κB p65: (1.34±0.07) folds vs. (1.86±0.11) folds when the expression in NS control group was represented as 1, all P < 0.05]. Conclusions Res cannot lower the mortality in mice with PQ poisoning, but it seems to be able to attenuate PQ-induced ALI and cell apoptosis. The mechanism responsible for the latter maybe the inhibitive effect of Res on NF-κB p65 translocation and cytokines production.

Aim To study the effects of extracellular acidosis on articular chondrocytes pyroptosis and its possible mechanisms. Methods Primary articular chondrocytes were incubated in different pH and NAC. The expression of proinflammatory cytokines IL-1β, IL-18, ASC, NLRP3, caspase-1 were detected by Western blot and real-time PCR. The state of pyropto-sis was identified by AO/EB staining and LDH con-tents. The expression of ROS was observed by DCFH-DA, and ELISA was used to detect the IL-1β,IL-18 in cultured supernatants. Results Compared with the normal cell, extracellular acidosis could increase the expression of IL-1β, IL-18, ASC, NLRP3 and caspase-1 , upregulate the fluorescence intensity of in-tercellular ROS, accompanied with the promoted release of LDH. Moreover, it is observed that extra-cellular acidosis could also induce chondrocytes death by AO/EB staining. NAC,the scavenger of ROS could inhibit these effects of extracellular acidosis on chon-drocytes. Conclusion Extracellular acidosis may in-duce chondrocyte pyroptosis via upregulating the intra-cellular ROS content.

Object To research and choose the best technology c onditions for extracting ursolic acid from Sambucus chinensis Li ndl. Methods According to physicochemical character of ursolic aci d, orthogonal design and tests of extract technology for ursolic acid were ca rried on, and four factors were chosen such as concentration, qu an tity of ethanol, extracting time, concentration of clearing agent, and three lev els of each factor were used for orthogonal design and test. Results That was the best technology condition that ursolic acid was extracted by means of ethyl alcohol (90%) of 7 times as much as raw materials, and it is heat ed 2 times (each 1 h), and the concentration of clearing agent was 3%. Conclusion That is a better technology for industrial producti on because it is advanced and rational, practical and feasible.

AIM:To investigate the effects of curcumin on cardiac dysfunction induced by chronic restraint stress in a depression rat model.METHODS:Thirty-two Wistar rats weighing(200±20)g were randomly divided into control,model,low-dose curcumin,and high-dose curcumin groups(n=8 per group).The rats in model and curcumin groups were subjected to chronic restraint stress for 5 h daily at random time,while those in control group were maintained under normal conditions.Following daily stress exposure,the rats in low-and high-dose curcumin groups received 100 and 200 mg/kg curcumin daily,respectively,and those in control and model groups received the same volume of normal saline daily.The above treatments lasted for 28 d.Body weight of the rats was measured weekly.Sucrose preference test was performed on days 14 and 28 of the experiment.Serum corticosterone content was determined to evaluate depression.Histological changes of cardiac tissues were observed using HE and Masson staining.Echocardiography was conducted to examine heart function.The related mRNA and protein levels were detected using RT-qPCR and Western blot,respective-ly.RESULTS:Compared with control group,the rats in model group exhibited significantly slower weight gain(P<0.05),impaired sucrose preference(P<0.01),and increased corticosterone levels(P<0.01).HE staining revealed myo-cardial hypertrophy in model group but not in control group.Masson staining indicated significantly higher cardiac fibrosis in model group than control group(P<0.01).Immunohistochemical staining demonstrated a significant increase in posi-tive collagen type I expression(P<0.01).RT-qPCR results showed significantly elevated mRNA levels of inflammatory cytokines(tumor necrosis factor-α,interleukin-6,and interleukin-1β)and fibrosis factors(α-smooth muscle actin,colla-gen type I,and collagen type Ⅲ)in model group compared with control group(P<0.05 or P<0.01).Western blot re-vealed a significant increase in c-Jun N-terminal kinase(JNK)phosphorylation level in model group(P<0.01).Treat-ment with low-and high-dose curcumin reversed the above indicators.CONCLUSION:Curcumin treatment attenuated cardiac inflammation and fibrosis in rats subjected to chronic restraint stress,possibly by inhibiting JNK signaling pathway.