Ipomoea aquatica (IA) with antioxidant properties is used in therapeutic trends. An organophosphate, dichlorvos (Dich), is a common insecticide with various side effects on living tissues. This study examines the role of IA on Dich-induced hepatotoxicity in male rats. Sixty-four male rats were divided into eight groups including sham, Dich (4 mg/kg/day, intraperitoneally), IA 1, 2, and 3 (250, 500, and 1000 mg/kg/day, respectively, orally), and Dich + IA 1, 2, and 3. All treatments were applied daily for 60 days. At the end of the treatment, the animals were sacrificed. The histopathological changes, leukocyte infiltration, and apoptosis were assessed by light and fluorescent microscopy. The serum levels of hepatic enzymes, nitrite oxide (NO), and total antioxidant capacity (TAC) were evaluated biochemically. Dich statistically significantly increased the NO level, hepatic enzyme activity, apoptosis, leukocyte infiltration, the mean diameter of hepatocytes (DHs), and central hepatic vein diameter (CHVD) and also decreased the TAC, mean weight of liver, and the total weight of rats compared to the sham group (P < 0.01). In all IA and Dich + IA groups, a statistically significant decrease was detected in apoptosis, leukocyte infiltration, hepatic enzyme activity, NO level, mean DH, and CHVD, whereas an increase in TAC level, mean liver weight, and total weight was detected compared to the Dich group (P < 0.01). IA, due to the antioxidant property, recovers the Dich-related catastrophic changes in liver.

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Repetitive hypoxic preconditioning (HP) enforces protective effects to subsequently severe hypoxic/ischemic stress. We hypothesized that HP may provide protection against ischemia/reperfusion (I/R) injury in rat livers via hypoxia-induced factor-1 alpha (HIF-1α)/reactive oxygen species (ROS)-dependent defensive mechanisms. Female Wistar rats were exposed to hypoxia (15 h/day) in a hypobaric hypoxic chamber (5500 m) for HP induction, whereas the others were kept in sea level. These rats were subjected to 45 min of hepatic ischemia by portal vein occlusion followed by 6 h of reperfusion. We evaluated HIF-1α in nuclear extracts, MnSOD, CuZnSOD, catalase, Bad/Bcl-xL/caspase 3/poly-(ADP-ribose)-polymerase (PARP), mitochondrial Bcl-xL, and cytosolic cytochrome C expression with Western blot and nitroblue tetrazolium/3-nitrotyrosine stain. Kupffer cell infiltration and terminal deoxynucleotidyl transferase-mediated nick-end labeling method apoptosis were determined by immunocytochemistry. The ROS value from liver surface and bile was detected by an ultrasensitive chemiluminescence–amplification method. Hepatic function was assessed with plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. HP increased nuclear translocation of HIF-1α and enhanced Bcl-xL, MnSOD, CuZnSOD, and catalase protein expression in a time-dependent manner. The response of HP enhanced hepatic HIF-1α, and Bcl-xL expression was abrogated by a HIF-1α inhibitor YC-1. Hepatic I/R increased ROS levels, myeloperoxidase activity, Kupffer cell infiltration, ALT and AST levels associated with the enhancement of cytosolic Bad translocation to mitochondria, release of cytochrome C to cytosol, and activation of caspase 3/PARP-mediated apoptosis. HP significantly ameliorated hepatic I/R-enhanced oxidative stress, apoptosis, and mitochondrial and hepatic dysfunction. In summary, HP enhances HIF-1α/ROS-dependent cascades to upregulate mitochondrial Bcl-xL protein expression and to confer protection against I/R injury in the livers.

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We investigated the expression of caveolin-1 (Cav-1) in Kawasaki disease (KD) and analyzed its relationship with coronary artery lesions (CALs). Cav-1 participated in the progression of CAL in KD. A total of 68 children with KD (23 with CALs), age matched with a fever control group (F, n = 28) and a normal control group (N, n = 24) were enrolled in this study. Cav-1 expression was detected using an enzyme-linked immunosorbent assay. The results are the following: (1) Compared with the F and N, Cav-1 expression was significantly increased in the children with KD (P < 0.05); there was no significant difference in Cav-1 between the F and N. (2) The serum level of Cav-1 was significantly higher in children with KD and CALs during the acute phase than in children with KD without CALs (P < 0.05). (3) Serum Cav-1 may be a biomarker that reflects CALs in children with KD based on a receiver operating characteristic (ROC) curve analysis. (4) Those children with KD who were given intravenous immunoglobulin (2 g/kg, 10–12 h) during the acute phase showed decreased expression of Cav-1 compared to the N. Conclusions are as follows: (1) The serum level of Cav-1 during the acute phase of KD increased significantly, while in KD patients with CALs the increase was even greater. (2) Based on our ROC curve analysis, Cav-1 may be a predictor of CALs in children with KD.

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Tectorigenin, a traditional Chinese medicine, is isolated from the flower of plants such as Pueraria thomsonii Benth. It is an O-methylated isoflavone, a type of flavonoid. Previous studies have shown that tectorigenin evoked various physiological responses in different models, but the effect of tectorigenin on cytosolic-free Ca²⁺ levels ([Ca²⁺]_i) and cytotoxicity in renal tubular cells is unknown. Our research explored if tectorigenin changed Ca²⁺ signal transduction and viability in Madin–Darby Canine Kidney (MDCK) renal tubular cells. [Ca²⁺]_i in suspended cells were measured by applying the fluorescent Ca²⁺-sensitive probe fura-2. Viability was explored by using water-soluble tetrazolium-1 as a fluorescent dye. Tectorigenin at concentrations of 5–50 μM induced [Ca²⁺]_i rises. Ca²⁺ removal reduced the signal by approximately 20%. Tectorigenin (50 μM) induced Mn²⁺ influx suggesting of Ca²⁺ entry. Tectorigenin-induced Ca²⁺ entry was inhibited by 10% by three inhibitors of store-operated Ca²⁺ channels, namely, nifedipine, econazole, and SKF96365. In Ca²⁺-free medium, treatment with the endoplasmic reticulum Ca²⁺ pump inhibitor thapsigargin inhibited 83% of tectorigenin-evoked [Ca²⁺]_i rises. Conversely, treatment with tectorigenin abolished thapsigargin-evoked [Ca²⁺]_i rises. Inhibition of phospholipase C with U73122 inhibited 50% of tectorigenin-induced [Ca²⁺]_i rises. Tectorigenin at concentrations between 10 and 60 μM killed cells in a concentration-dependent fashion. Chelation of cytosolic Ca²⁺ with 1,2-bis (2-aminophenoxy)ethane-N, N, N', N'-tetraacetic acid/acetoxy methyl did not reverse tectorigenin's cytotoxicity. Our data suggest that, in MDCK cells, tectorigenin evoked [Ca²⁺]_i rises and induced cell death that was not associated with [Ca²⁺]_i rises. Therefore, tectorigenin may be a Ca²⁺-independent cytotoxic agent for kidney cells.

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Water-induced pressor response appears mediated through the activation of transient receptor potential channel TRPV4 on hepatic portal circulation in animals. We sought to elucidate the mechanism of portal vein signaling in this response. Forty-five rats were divided into four groups: control rats without water ingestion (WI), control rats with WI, portal vein denervation rats with WI (PVDWI), and TRPV4 antagonist-treated rats with WI (anti-TRPV4WI). Cardiovascular responses were monitored throughout the experiments. Data analysis was performed using descriptive methods and spectral and cross-spectral analysis of blood pressure variability (BPV) and heart rate variability (HRV). Key results showed that at baseline (PreCS) before cold stress trial (CS), WI elicited robust pressor and tachycardia responses accompanied by spectral power changes, in particular, increases of low-frequency BPV (LFBPV) and very-LFBPV (VLFBPV), but decrease of very-low-frequency HRV. PVDWI, likewise, elicited pressor and tachycardia responses accompanied by increases of high-frequency BPV, high-frequency HRV, LFBPV, low-frequency HRV, and VLFBPV. When compared with WI at PreCS, WI at CS elicited pressor and tachycardia responses accompanied by increases of high-frequency BPV, LFBPV, and VLFBPV, whereas in WI, the CS-evoked pressor response and the accompanied LFBPV and VLFBPV increases were all tended augmented by PVDWI. When compared with WI and PVDWI at both PreCS and CS, however, anti-TRPV4WI attenuated their pressor responses and attenuated their increased LFBPV, VLFBPV, and very-low-frequency HRV. The results indicate that the portal vein innervation is critical for a buffering mechanism in splanchnic sympathetic activation and water-induced pressor response.

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The purpose of this study was to investigate muscle activity and intermuscular coherence of the rectus femoris (RF) and biceps femoris (BF) during forward (FW) and backward (BW) pedaling. Sixteen healthy volunteers performed FW and BW pedaling in 30, 45, and 60 revolutions per minute (RPM), while electromyographic (EMG) signals of the RF and BF were recorded bilaterally to determine integral EMG and intermuscular coherence. BW pedaling showed a statistically significant larger EMG activity on the left BF (P = 0.023) in 30 RPM; on the left BF (P = 0.01), right BF (P = 0.05), and right RF (P = 0.006) in 45 RPM, and on the left BF (P = 0.014) and right RF (P = 0.011) in 60 RPM than FW pedaling. In 45 RPM, higher coherence was demonstrated on the left leg (P = 0.011) during the left flexor and right extensor phases and on the right leg (P = 0.043) during the right flexor and left extensor phases in BW compared with FW pedaling. In 60 RPM, higher coherence was observed on both legs (left, P = 0.037; right, P < 0.001) during the left flexor and right extensor phases in BW compared with FW pedaling. Our results suggest that BW pedaling increased the muscle activity of both biarticular muscles and intermuscular coherence.

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