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Objective To summarize the experience of the prevention and treatment of iatrogenic hypo-parathyroidism in total thyroidectomy .Methods 377 patients received total thyroidectomy performed by the Thy-roid Professional Group of Hepatobiliary Surgery Department of the Third Affiliated Hospital of Soochow University from Jan.2010 to Dec.2012.Their clinical date were retrospectively analyzed .Results There was no perma-nent postoperative hypoparathyroidism .The incidence of temporary hypoparathyroidism was 13.79%( 52/377 ) . The occurrence of transient hypocalcemia was 10.61%( 40/377 ) .Conclusions Iatrogenic hypoparathyroidism can be prevented by intraoperative in situ protection of parathyroid glands and their blood supply using fine cap -sule anatomy method .Postoperative improvement of microcirculation and calcium supplement also help prevent postoperative hypoparathyroidism .
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ObjectiveTo investigate the protective effect of astragalosideⅣ pretreatment against liver ischemia/reperfusion (I/R) injury in mice.MethodsSixty male C57BL/6 mice were randomized into four groups (15 mice in each group):group A:sham surgery with saline injection,group B:sham surgery with astragalosideⅣ injection,group C:I/R group with saline injection,group D:I/R and astragalosideⅣ injection.Mice were pretreated by daily intraperitoneal injection of saline or astragalosideⅣ (24 mg · kg-1 · d-1 ) for one week.The mouse partial liver model of I/R injury was established,and samples were collected at the 24 h after the I/R injury.Serum ALT and AST levels were determined,the histologic changes were observed by H&E staining under the light microscopy,whereas the nuclear factor (NF)-κB was assessed with Western blotting.Serum IL-1β,IL-6,and TNF-α levels were measured by enzyme-linked immunosorbent assay (ELISA). ResultsSerum ALT and AST levels significantly decreased and the histological damage was significantly alleviated in astragalosideⅣ treated I/R group as compared with saline I/R group [ AST:C:(4290± 292) U/L vs.D:(2373± 416) U/L t =0.844 ; ALT:C:(4146±500) U/L vs.D:(2318±289) U/L t =7.08 P ＜0.05].In comparison with group 3,astragalosideⅣ reduced NF-κB nuclear expression.ELISA showed astragalosideⅣ significantly inhibit the levels of IL-1 β,IL-6,and TNF-α in the serum (IL-1β:t =10.04;IL-6:t =6.281;TNF-α:t =6.817; P ＜0.05).ConclusionsPretreatment with astragaloside Ⅳ effectively protect against liver ischemia/reperfusion injury in mice.
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ObjectiveTo investigate the effect and related mechanism of triptolide pretreatment to prevent from ischemia/reperfusion (I/R) injury in mice liver. MethodsSixty male C57BL/6 mouse were randomized into four groups (15/group): A:sham group with saline , B: sham group with triptolide, C: saline I/R group, D: triptolide I/R group. The mice were pretreated with either saline or triptolide (0. 1 mg/kg/d) through intraperitoneal (ip) injection for one week. The mouse partial liver model of I/R injury was established, and samples were collected at 24 h after the I/R injury. ResultsSerum ALT and AST levels were significantly decreased and histological damage was significantly alleviated in the triptolide I/R group as compared with the saline I/R group (P＜0.05), the concentration of MDA in the triptolide groups was significantly decreased, while SOD activity was significantly increased compared with that of the saline I/R group (P＜0.05). The percentages of CD4+ CD25+ regulatory T cells (Tregs) cells among CD4+ T cells in groups A, B, C, and D were(7. 55 ± 1.87)%, (12. 59±3. 87)%,(7. 85±1.07)%, and(12. 02±3. 16)% in liver tissue, respectively. The expression levels of Foxp3 mRNA were significantly higher in the triptolide I/R group than those of saline I/R group (P＜0. 05). ELISA showed that triptolide could significantly inhibit the levels of IL-6, IL-Iβ and TNF-αand promoted the level of IL-10 in the serum (P＜0.05). Conclusion Pretreatment with triptolide could effectively prevent from liver I/R injury, which may be related to the induction of Treg cells by triptolide, the increase in the level of IL-10 in serum, and the inhibition of IL-6, IL-1β and TNF-α production in serum.
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Objective To investigate the protective effect of triptolide (TPT) pretreatment against liver ischemia/reperfusion (I/R) injury in mice and the possible mechanism. Methods Sixty male C57BL/6 mice were randomly divided into four groups (15/group): ( 1 ) TPT I/R group: The mouse partial liver model of I/R injury was established by the method of Koba-yashi. The portal triad (hepatic artery, portal vein, and bile duct) was occluded with a microvascular clamp for 90 min and 24 h reperfusion; (2) Sham group with TPT: Mice underwent surgical procedures including isolation of the portal triad without occlusion; (3) Saline I/R group: Surgery was performed as the same in the TPT I/R group, (4): Sham group with saline: Surgery was performed as the same in the TPT sham group, and the mice were pretreated with either saline or TPT (0. 1 mg · kg-1 day-1 ) by intraperitoneal injection for one week. The samples were collected at the 24th h after the I/R injury.The serum ALT and AST levels were determined, the histologic changes were observed by HE staining, the percentage of Th17 cells among mononuclear cells in liver tissue was analyzed by flow cytometry, the expression of IL-17 and ROR-γt mRNA was detected by real-time PCR, and the serum IL-6, IL-17 and TGF-β levels were measured by enzyme-linked immunosorbent assay (ELISA).Results Serum ALT and AST levels were significantly decreased and the histological damage was significantly alleviated in the TPT I/R group as compared with saline I/R group (P＜0. 05). The percentage of Th17 cells among mononuclear cells in TPT I/R group, TPT sham group, saline I/R group, TPT saline group was ( 1.77 ± 0. 53)％, (0. 41± 0. 18)％, (4. 26 ± 0. 82)％ and (0. 72 ± 0. 23) ％ in liver tissue, respectively. The expression levels of the IL-17 and ROR-γt mRNA in the liver tissue, and IL-6, IL-17 and TGF-β levels in the serum were significantly lower in TPT I/R group than in saline I/R group (P＜0. 05). Conclusion Pretreatment with low dose of TPT could effectively protect the liver from I/R injury in mice, which may be related to the inhibition of Th17 cells.