OBJECTIVETo explore the regulation and clinical significance of intestinal dripping of Jianpi Tongli (JPTL) Chinese herbs on levels of serum cytokines, such as interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R) and interleukin-12 (IL-12) in treating patients with gastric cancer (GC) at early post-operational stage.

METHODSSixty patients with GC were randomly divided into two groups, i. e. the studied group (n = 30), treated with JPTL Chinese herbs, and the control group (n = 30) treated with normal saline. The medication was started from the 1st day after operation by intestinal dripping daily, 7 days as one course. Levels of IL-2, sIL-2R and IL-12 were observed before and after operation.

RESULTSSignificant difference was seen on the 7th day post-operation between the studied and the control group, mainly in aspects of obvious increase of IL-2 and decrease of sIL-2R (P <0.05), no significant difference in IL-12 was found (P >0.05) though there was certain improvement. Compared with pre-operation of the same group, significant difference was found in the studied group in the increased IL-2 and IL-12 and decreased sIL-2R on the 7th day post-operation, while no significant difference in these indexes was found in the control group (P >0.05), though certain improvement was shown.

CONCLUSIONEarly intestinal dripping of JPTL Chinese herbs to post-operational patients with GC could improve their immune function, which was of important significance in early preventing the severe complications, improving the prognosis, and elevating the survival rate.

Adenocarcinoma ; blood ; drug therapy ; surgery ; Adult ; Aged ; Combined Modality Therapy ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Humans ; Interleukin-12 ; blood ; Interleukin-2 ; blood ; Intestine, Small ; Intubation, Gastrointestinal ; Male ; Middle Aged ; Phytotherapy ; Postoperative Period ; Receptors, Interleukin-2 ; blood ; Stomach Neoplasms ; blood ; drug therapy ; surgery

Objective To investigate the relationship between the interleukin (IL)-35 and the recovery of renal graft function. Methods Clinical data of 45 recipients receiving renal transplantation from donation after cardiac death (DCD) were retrospectively analyzed. According to the presence of delayed graft function (DGF) after renal transplantation, all recipients were divided into the immediate graft function (IGF) group (n=32) and DGF group (n=13). The serum creatinine (Scr) level and estimated glomerular filtration rate (eGFR) in the recipients were statistically compared between two groups at 1, 2, 3, 7, 14, 28 d and 3, 6 and 12 months after renal transplantation. The IL-35 levels in the serum and urine samples of the recipients were statistically compared between two groups at 1, 2, 3, 7, 14, 28 d following renal transplantation. Results In the DGF group, the renal function was restored slowly. Compared with the IGF group, the Scr level was significantly higher, whereas the eGFR was considerably lower in the DGF group at postoperative 7 d (both P<0.05). At 1 year after surgery, there was no significant difference in the Scr level between two groups. Compared with the IGF group, the eGFR in the DGF group was significantly lower at postoperative 1 year (P<0.05). At 1, 2, 3, 7, 14 d after operation, the serum levels of IL-35 in the DGF group were evidently lower than those in the IGF group (all P<0.05). Compared with the IGF group, the serum level of IL-35 in the DGF group was significantly increased at postoperative 28 d (P<0.05). At postoperative 1, 2, 3, 7 d, the IL-35 levels in the urine samples in the DGF group were significantly lower than those in the IGF group (all P<0.05). At postoperative 14 and 28 d, the IL-35 levels in the urine samples did not significantly differ between two groups (both P>0.05). Conclusions The low levels of IL-35 in the serum and urine of recipients after renal transplantation are associated with the incidence of DGF to certain extent, prompting that excessively weak systemic and local anti-inflammatory responses early after renal transplantation and uncontrolled excessive inflammatory response are probably the pivotal causes of DGF.

Objective To investigate the antagonism of third generation dihydropyridine calcium channel antagonist beni-dipine in contraction induced by potassium chloride(KCl)in human internal mammary artery(IMA),and in order to explore the possibility of using benidipine as an antispastic agent during coronary artery bypass grafting(CABG). Methods The IMAs were taken from 19 patients undergoing CABG. The vasodilator effect(n = 7)on KCl-induced contraction and the inhibition effect(n = 6)after incubation with benidipine were studied in a myograph. The caveolin 1. 2 was detected(n = 3,2 cases re-spectively)by enzyme-linked immunosorbent assay (ELISA). Results The maximum relaxation caused benidipine was (87. 7 ± 4. 9)％ . Incubation with benidipine significantly depressed the contraction by KCl[from( 16. 9 ± 4. 4)mN to (9. 1 ± 3. 4 )mN,P < 0. 01]. The concentration of caveolin 1. 2 was down-regulated after incubation with benidipine(P < 0. 05). Conclusion Benidipine has a potent inhibitory effect on KCl-induced vasoconstriction. The relaxation may be related with the expression of caveolin 1. 2. Using benidipine in patients undergoing CABG may provide antispastic effects in grafts.

A neuroinflammatory response is commonly involved in the progression of many neurodegenerative diseases. Potassium 2-(1-hydroxypentyl)-benzoate (PHPB), a novel neuroprotective compound, has shown promising effects in the treatment of ischemic stroke and Alzheimer׳s disease (AD). In the present study, the anti-inflammatory effects of PHPB were investigated in the plasma and brain of C57BL/6 mice administered a single intraperitoneal (i.p.) injection of lipopolysaccharide (LPS). Levels of iNOS and the cytokines TNF, IL-1and IL-10 were elevated in plasma, cerebral cortex and hippocampus after LPS injection and the number of microglia and astrocytes in cortex and hippocampus were increased. LPS also upregulated the expression of heme oxygenase-1 (HO-1) in the cortex and hippocampus. PHPB reduced the levels of iNOS and cytokines in the plasma and brain, decreased the number of microglia and astrocytes and further enhanced the upregulation of HO-1. In addition, PHPB inhibited the LPS-induced phosphorylation of ERK, P38 and JNK. These results suggest that PHPB is a potential candidate in the treatment of neurodegenerative diseases through inhibiting neuroinflammation.